Oral cancer ranks among the most common malignancies within the head and neck region; however, its etiology remains inadequately understood despite substantial research advances in recent years. Many studies highlight the regulatory role of circular RNAs (circRNAs) in human cancers, suggesting their potential as cancer biomarkers. However, their specific mechanisms in oral cancer are not well understood. This study analyzed circRNAs expression in oral cancer, identifying circRNF13 (circbaseID: has_circ_0006801) as having elevated expression in oral cancer cells and tissues. Our study demonstrated that circRNF13 is correlated with increased tumor grade and stage in oral cancer. Results from both in vitro and in vivo experiments indicated that circRNF13 enhances cancer cell proliferation and tumor growth, while concurrently diminishing tumor sensitivity to cisplatin. Mechanistically, circRNF13 interacts with the m6A “reader” protein IGF2BP1, inhibiting its ubiquitin-mediated degradation and promoting its phase separation formation. Subsequently, circRNF13 augments the stability of ITGB1 mRNA via IGF2BP1 in a manner dependent on m6A modification. The m6A modification of ITGB1 mRNA is modulated by the phase separation of IGF2BP1, thereby promoting the malignant progression of oral cancer cells. This evidence positions circRNF13 as a crucial regulatory molecule in the pathogenesis of oral cancer and suggests its potential as a therapeutic target. This discovery enriches our understanding of the mechanistic role of circRNAs.
{"title":"CircRNF13 enhances IGF2BP1 phase separation-mediated ITGB1 mRNA stabilization in an m6A-dependent manner to promote oral cancer cisplatin chemoresistance","authors":"Xuemeng Xu, Qiu Peng, Zongyao Ren, Yaqian Han, Xianjie Jiang, Zhu Wu, Shiming Tan, Wenjuan Yang, Linda Oyang, Xia Luo, Jinguan Lin, Longzheng Xia, Mingjing Peng, Nayiyuan Wu, Yanyan Tang, Hao Tian, Yujuan Zhou, Qianjin Liao","doi":"10.1186/s12943-025-02239-4","DOIUrl":"https://doi.org/10.1186/s12943-025-02239-4","url":null,"abstract":"Oral cancer ranks among the most common malignancies within the head and neck region; however, its etiology remains inadequately understood despite substantial research advances in recent years. Many studies highlight the regulatory role of circular RNAs (circRNAs) in human cancers, suggesting their potential as cancer biomarkers. However, their specific mechanisms in oral cancer are not well understood. This study analyzed circRNAs expression in oral cancer, identifying circRNF13 (circbaseID: has_circ_0006801) as having elevated expression in oral cancer cells and tissues. Our study demonstrated that circRNF13 is correlated with increased tumor grade and stage in oral cancer. Results from both in vitro and in vivo experiments indicated that circRNF13 enhances cancer cell proliferation and tumor growth, while concurrently diminishing tumor sensitivity to cisplatin. Mechanistically, circRNF13 interacts with the m6A “reader” protein IGF2BP1, inhibiting its ubiquitin-mediated degradation and promoting its phase separation formation. Subsequently, circRNF13 augments the stability of ITGB1 mRNA via IGF2BP1 in a manner dependent on m6A modification. The m6A modification of ITGB1 mRNA is modulated by the phase separation of IGF2BP1, thereby promoting the malignant progression of oral cancer cells. This evidence positions circRNF13 as a crucial regulatory molecule in the pathogenesis of oral cancer and suggests its potential as a therapeutic target. This discovery enriches our understanding of the mechanistic role of circRNAs.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"128 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143072130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p><b>Correction</b>: <b><i>Mol Cancer</i></b><b> 23</b>,<b> 186 (2024)</b></p><p><b>https://doi.org/10.1186/s12943-024-02097-6</b></p><p>Following publication of the original article [1], it was noted that the authors inadvertently left out the major funding source in the Funding information section, which was highly dependent throughout the study. Therefore, they requested to update the information under the Funding section. The original article has been corrected.</p><p> The Funding information currently reads:</p><p> <b>Fundings</b></p><p>This work is funded by the National Natural Science Foundation of China (No: 81874070 to M.S. Chen, 82073243 to X. Wang, 82103566 to D.D. Hu ), Guangdong Basic and Applied Basic Research Foundation (2022A1515110961 to J.C. Wang), Guangzhou Science and Technology Plan Project (2023A04J2125 to J.C. Wang), the China Postdoctoral Science Foundation (No: 2023M744018 to Y.Z. Fu).</p><p> The Funding information should read:</p><p> <b>Fundings</b></p><p>This work is funded by the Guangdong Provincial Science Fund for Distinguished Young Scholars (2021B1515020007, to J.Hou), the National Natural Science Foundation of China (No: 81874070 to M.S. Chen, 82073243 to X. Wang, 82103566 to D.D. Hu), Guangdong Basic and Applied Basic Research Foundation (2022A1515110961 to J.C. Wang), Guangzhou Science and Technology Plan Project (2023A04J2125 to J.C. Wang), the China Postdoctoral Science Foundation (No: 2023M744018 to Y.Z. Fu).</p><ol data-track-component="outbound reference" data-track-context="references section"><li data-counter="1."><p>Yang Z, Wang X, Fu Y, et al. YTHDF2 in peritumoral hepatocytes mediates chemotherapy-induced antitumor immune responses through CX3CL1-mediated CD8<sup>+</sup> T cell recruitment. Mol Cancer. 2024;23:186. https://doi.org/10.1186/s12943-024-02097-6.</p><p>Article CAS PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden="true" focusable="false" height="16" role="img" width="16"><use xlink:href="#icon-eds-i-download-medium" xmlns:xlink="http://www.w3.org/1999/xlink"></use></svg></p><h3>Authors and Affiliations</h3><ol><li><p>Department of Liver Surgery, Sun Yat-sen University Cancer Center, Guangzhou, 510060, Guangdong, People’s Republic of China</p><p>Zhenyun Yang, Xin Wang, Yizhen Fu, Weijie Wu, Zili Hu, Qingyang Lin, Wei Peng, Yangxun Pan, Juncheng Wang, Jinbin Chen, Dandan Hu, Zhongguo Zhou, Li Xu, Yaojun Zhang & Minshan Chen</p></li><li><p>Collaborative Innovation Center for Cancer Medicine, State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, Guangdong, People’s Republic of China</p><p>Zhenyun Yang, Xin Wang, Yizhen Fu, Weijie Wu, Zili Hu, Qingyang Lin, Wei Peng, Yangxun Pan, Juncheng Wang, Jinbin Chen, Dandan Hu, Zhongguo Zhou, Li Xu, Yaojun Zhang & Minshan Chen</p></li><li><p>State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Collab
{"title":"Correction: YTHDF2 in peritumoral hepatocytes mediates chemotherapy-induced antitumor immune responses through CX3CL1-mediated CD8+ T cell recruitment","authors":"Zhenyun Yang, Xin Wang, Yizhen Fu, Weijie Wu, Zili Hu, Qingyang Lin, Wei Peng, Yangxun Pan, Juncheng Wang, Jinbin Chen, Dandan Hu, Zhongguo Zhou, Li Xu, Yaojun Zhang, Jiajie Hou, Minshan Chen","doi":"10.1186/s12943-025-02252-7","DOIUrl":"https://doi.org/10.1186/s12943-025-02252-7","url":null,"abstract":"<p><b>Correction</b>: <b><i>Mol Cancer</i></b><b> 23</b>,<b> 186 (2024)</b></p><p><b>https://doi.org/10.1186/s12943-024-02097-6</b></p><p>Following publication of the original article [1], it was noted that the authors inadvertently left out the major funding source in the Funding information section, which was highly dependent throughout the study. Therefore, they requested to update the information under the Funding section. The original article has been corrected.</p><p> The Funding information currently reads:</p><p>\u0000<b>Fundings</b></p><p>This work is funded by the National Natural Science Foundation of China (No: 81874070 to M.S. Chen, 82073243 to X. Wang, 82103566 to D.D. Hu ), Guangdong Basic and Applied Basic Research Foundation (2022A1515110961 to J.C. Wang), Guangzhou Science and Technology Plan Project (2023A04J2125 to J.C. Wang), the China Postdoctoral Science Foundation (No: 2023M744018 to Y.Z. Fu).</p><p> The Funding information should read:</p><p>\u0000<b>Fundings</b></p><p>This work is funded by the Guangdong Provincial Science Fund for Distinguished Young Scholars (2021B1515020007, to J.Hou), the National Natural Science Foundation of China (No: 81874070 to M.S. Chen, 82073243 to X. Wang, 82103566 to D.D. Hu), Guangdong Basic and Applied Basic Research Foundation (2022A1515110961 to J.C. Wang), Guangzhou Science and Technology Plan Project (2023A04J2125 to J.C. Wang), the China Postdoctoral Science Foundation (No: 2023M744018 to Y.Z. Fu).</p><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Yang Z, Wang X, Fu Y, et al. YTHDF2 in peritumoral hepatocytes mediates chemotherapy-induced antitumor immune responses through CX3CL1-mediated CD8<sup>+</sup> T cell recruitment. Mol Cancer. 2024;23:186. https://doi.org/10.1186/s12943-024-02097-6.</p><p>Article CAS PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></p><h3>Authors and Affiliations</h3><ol><li><p>Department of Liver Surgery, Sun Yat-sen University Cancer Center, Guangzhou, 510060, Guangdong, People’s Republic of China</p><p>Zhenyun Yang, Xin Wang, Yizhen Fu, Weijie Wu, Zili Hu, Qingyang Lin, Wei Peng, Yangxun Pan, Juncheng Wang, Jinbin Chen, Dandan Hu, Zhongguo Zhou, Li Xu, Yaojun Zhang & Minshan Chen</p></li><li><p>Collaborative Innovation Center for Cancer Medicine, State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, Guangdong, People’s Republic of China</p><p>Zhenyun Yang, Xin Wang, Yizhen Fu, Weijie Wu, Zili Hu, Qingyang Lin, Wei Peng, Yangxun Pan, Juncheng Wang, Jinbin Chen, Dandan Hu, Zhongguo Zhou, Li Xu, Yaojun Zhang & Minshan Chen</p></li><li><p>State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Collab","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"41 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143071852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-31DOI: 10.1186/s12943-025-02236-7
Mila Gugnoni, Manoj Kumar Kashyap, Kishore K. Wary, Alessia Ciarrocchi
Cancer progression relies on the ability of cells to adapt to challenging environments overcoming stresses and growth constraints. Such adaptation is a multifactorial process that depends on the rapid reorganization of many basic cellular mechanisms. Protein synthesis is often dysregulated in cancer, and translational reprogramming is emerging as a driving force of cancer adaptive plasticity. Long non-coding RNAs (lncRNAs) represent the main product of genome transcription. They outnumber mRNAs by an order of magnitude and their expression is regulated in an extremely specific manner depending on context, space and time. This heterogeneity is functional and allows lncRNAs to act as context-specific, fine-tuning controllers of gene expression. Multiple recent evidence underlines how, besides their consolidated role in transcription, lncRNAs are major players in translation control. Their capacity to establish multiple and highly dynamic interactions with proteins and other transcripts makes these molecules able to play a central role across all phases of protein synthesis. Even if through a myriad of different mechanisms, the action of these transcripts is dual. On one hand, by modulating the overall translation speed, lncRNAs participate in the process of metabolic adaptation of cancer cells under stress conditions. On the other hand, by prioritizing the synthesis of specific transcripts they help cancer cells to maintain high levels of essential oncogenes. In this review, we aim to discuss the most relevant evidence regarding the involvement of lncRNAs in translation regulation and to discuss how this specific function may affect cancer plasticity and resistance to stress. We also expect to provide one of the first collective perspectives on the way these transcripts modulate gene expression beyond transcription.
{"title":"lncRNAs: the unexpected link between protein synthesis and cancer adaptation","authors":"Mila Gugnoni, Manoj Kumar Kashyap, Kishore K. Wary, Alessia Ciarrocchi","doi":"10.1186/s12943-025-02236-7","DOIUrl":"https://doi.org/10.1186/s12943-025-02236-7","url":null,"abstract":"Cancer progression relies on the ability of cells to adapt to challenging environments overcoming stresses and growth constraints. Such adaptation is a multifactorial process that depends on the rapid reorganization of many basic cellular mechanisms. Protein synthesis is often dysregulated in cancer, and translational reprogramming is emerging as a driving force of cancer adaptive plasticity. Long non-coding RNAs (lncRNAs) represent the main product of genome transcription. They outnumber mRNAs by an order of magnitude and their expression is regulated in an extremely specific manner depending on context, space and time. This heterogeneity is functional and allows lncRNAs to act as context-specific, fine-tuning controllers of gene expression. Multiple recent evidence underlines how, besides their consolidated role in transcription, lncRNAs are major players in translation control. Their capacity to establish multiple and highly dynamic interactions with proteins and other transcripts makes these molecules able to play a central role across all phases of protein synthesis. Even if through a myriad of different mechanisms, the action of these transcripts is dual. On one hand, by modulating the overall translation speed, lncRNAs participate in the process of metabolic adaptation of cancer cells under stress conditions. On the other hand, by prioritizing the synthesis of specific transcripts they help cancer cells to maintain high levels of essential oncogenes. In this review, we aim to discuss the most relevant evidence regarding the involvement of lncRNAs in translation regulation and to discuss how this specific function may affect cancer plasticity and resistance to stress. We also expect to provide one of the first collective perspectives on the way these transcripts modulate gene expression beyond transcription.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"27 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143071858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-31DOI: 10.1186/s12943-025-02251-8
Claire Corcoran, Sweta Rani, Susan Breslin, Martina Gogarty, Irene M Ghobrial, John Crown, Lorraine O’Driscoll
<p><b>Correction</b><b>: </b><b>Mol Cancer 13, 71 (2014)</b></p><p><b>https://doi.org/10.1186/1476-4598-13-71</b></p><br/><p>Following the publication of the original article [1], the authors would like to update Figure 4 as the SKBR3-LR NC mimic migration image presented in the published article was incorrect, but the associated graph showing % fold change was correct. The error was due to a pasting error when compiling the composite figure (two NC mimic invasion images were inadvertently pasted, instead of one NC mimic migration and one NC mimic invasion image). The incorrect and correct figures are provided below.</p><p>Incorrect Figure 4:</p><figure><picture><source srcset="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02251-8/MediaObjects/12943_2025_2251_Figa_HTML.png?as=webp" type="image/webp"/><img alt="figure a" aria-describedby="Figa" height="535" loading="lazy" src="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02251-8/MediaObjects/12943_2025_2251_Figa_HTML.png" width="685"/></picture></figure><p>Correct Figure 4:</p><figure><picture><source srcset="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02251-8/MediaObjects/12943_2025_2251_Figb_HTML.png?as=webp" type="image/webp"/><img alt="figure b" aria-describedby="Figb" height="532" loading="lazy" src="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02251-8/MediaObjects/12943_2025_2251_Figb_HTML.png" width="685"/></picture></figure><ol data-track-component="outbound reference" data-track-context="references section"><li data-counter="1."><p>Corcoran C, Rani S, Breslin S, et al. miR-630 targets IGF1R to regulate response to HER-targeting drugs and overall cancer cell progression in HER2 over-expressing breast cancer. Mol Cancer. 2014;13:71. https://doi.org/10.1186/1476-4598-13-71.</p><p>Article CAS PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden="true" focusable="false" height="16" role="img" width="16"><use xlink:href="#icon-eds-i-download-medium" xmlns:xlink="http://www.w3.org/1999/xlink"></use></svg></p><h3>Authors and Affiliations</h3><ol><li><p>School of Pharmacy and Pharmaceutical Sciences & Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland</p><p>Claire Corcoran, Sweta Rani, Susan Breslin, Martina Gogarty & Lorraine O’Driscoll</p></li><li><p>Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA</p><p>Irene M Ghobrial</p></li><li><p>Department of Oncology, St. Vincent’s University Hospital, Dublin 4, Ireland</p><p>John Crown</p></li></ol><span>Authors</span><ol><li><span>Claire Corcoran</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Sweta Rani</span>View author publications<p>You can also search for this author in <span>PubMed<span>
{"title":"Correction: miR-630 targets IGF1R to regulate response to HER-targeting drugs and overall cancer cell progression in HER2 over-expressing breast cancer","authors":"Claire Corcoran, Sweta Rani, Susan Breslin, Martina Gogarty, Irene M Ghobrial, John Crown, Lorraine O’Driscoll","doi":"10.1186/s12943-025-02251-8","DOIUrl":"https://doi.org/10.1186/s12943-025-02251-8","url":null,"abstract":"<p><b>Correction</b><b>: </b><b>Mol Cancer 13, 71 (2014)</b></p><p><b>https://doi.org/10.1186/1476-4598-13-71</b></p><br/><p>Following the publication of the original article [1], the authors would like to update Figure 4 as the SKBR3-LR NC mimic migration image presented in the published article was incorrect, but the associated graph showing % fold change was correct. The error was due to a pasting error when compiling the composite figure (two NC mimic invasion images were inadvertently pasted, instead of one NC mimic migration and one NC mimic invasion image). The incorrect and correct figures are provided below.</p><p>Incorrect Figure 4:</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02251-8/MediaObjects/12943_2025_2251_Figa_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure a\" aria-describedby=\"Figa\" height=\"535\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02251-8/MediaObjects/12943_2025_2251_Figa_HTML.png\" width=\"685\"/></picture></figure><p>Correct Figure 4:</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02251-8/MediaObjects/12943_2025_2251_Figb_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure b\" aria-describedby=\"Figb\" height=\"532\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02251-8/MediaObjects/12943_2025_2251_Figb_HTML.png\" width=\"685\"/></picture></figure><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Corcoran C, Rani S, Breslin S, et al. miR-630 targets IGF1R to regulate response to HER-targeting drugs and overall cancer cell progression in HER2 over-expressing breast cancer. Mol Cancer. 2014;13:71. https://doi.org/10.1186/1476-4598-13-71.</p><p>Article CAS PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></p><h3>Authors and Affiliations</h3><ol><li><p>School of Pharmacy and Pharmaceutical Sciences & Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland</p><p>Claire Corcoran, Sweta Rani, Susan Breslin, Martina Gogarty & Lorraine O’Driscoll</p></li><li><p>Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA</p><p>Irene M Ghobrial</p></li><li><p>Department of Oncology, St. Vincent’s University Hospital, Dublin 4, Ireland</p><p>John Crown</p></li></ol><span>Authors</span><ol><li><span>Claire Corcoran</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Sweta Rani</span>View author publications<p>You can also search for this author in <span>PubMed<span>","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"24 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143072128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-30DOI: 10.1186/s12943-025-02232-x
Diogo Coelho, Diogo Estêvão, Maria José Oliveira, Bruno Sarmento
Rectal cancer accounts for over 35% of the worldwide colorectal cancer burden representing a distinctive subset of cancers from those arising in the colon. Colorectal cancers exhibit a continuum of traits that differ with their location in the large intestine. Due to anatomical and molecular differences, rectal cancer is treated differently from colon cancer, with neoadjuvant chemoradiotherapy playing a pivotal role in the control of the locally advanced disease. However, radioresistance remains a major obstacle often correlated with poor prognosis. Multifunctional nanomedicines offer a promising approach to improve radiotherapy response rates, as well as to increase the intratumoral concentration of chemotherapeutic agents, such as 5-Fluorouracil. Here, we revise the main molecular differences between rectal and colon tumors, exploring the complex orchestration beyond rectal cancer radioresistance and the most promising nanomedicines reported in the literature to improve neoadjuvant therapy response rates.
{"title":"Radioresistance in rectal cancer: can nanoparticles turn the tide?","authors":"Diogo Coelho, Diogo Estêvão, Maria José Oliveira, Bruno Sarmento","doi":"10.1186/s12943-025-02232-x","DOIUrl":"https://doi.org/10.1186/s12943-025-02232-x","url":null,"abstract":"Rectal cancer accounts for over 35% of the worldwide colorectal cancer burden representing a distinctive subset of cancers from those arising in the colon. Colorectal cancers exhibit a continuum of traits that differ with their location in the large intestine. Due to anatomical and molecular differences, rectal cancer is treated differently from colon cancer, with neoadjuvant chemoradiotherapy playing a pivotal role in the control of the locally advanced disease. However, radioresistance remains a major obstacle often correlated with poor prognosis. Multifunctional nanomedicines offer a promising approach to improve radiotherapy response rates, as well as to increase the intratumoral concentration of chemotherapeutic agents, such as 5-Fluorouracil. Here, we revise the main molecular differences between rectal and colon tumors, exploring the complex orchestration beyond rectal cancer radioresistance and the most promising nanomedicines reported in the literature to improve neoadjuvant therapy response rates. ","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"4 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143056476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sorafenib, an FDA-approved drug for advanced hepatocellular carcinoma (HCC), faces resistance issues, partly due to myeloid-derived suppressor cells (MDSCs) that enhance immunosuppression in the tumor microenvironment (TME). Various murine HCC cell lines and MDSCs were used in a series of in vitro and in vivo experiments. These included subcutaneous tumor models, cell viability assays, flow cytometry, immunohistochemistry, and RNA sequencing. MDSCs were analyzed for chemotaxis, immunosuppressive functions, fatty acid oxidation (FAO), and PPARα expression. The impact of sorafenib on tumor growth, MDSC infiltration, differentiation, and immunosuppressive function was assessed, alongside the modulation of these processes by PPARα. Here, we revealed increased infiltration and enhanced function of MDSCs in TME after treatment with sorafenib. Moreover, our results indicated that sorafenib induced the accumulation of MDSCs mediated by CCR2, and pharmacological blockade of CCR2 markedly reduced MDSCs migration and tumor growth. Mechanistically, sorafenib promoted the effect and fatty acid uptake ability of MDSCs and modulated peroxisome proliferator-activated receptor α (PPARα)-mediated fatty acid oxidation (FAO). In addition, tumor-bearing mice fed a high-fat diet (HFD) at the beginning of sorafenib administration had worse outcomes than mice fed a regular diet. Genetic deficiency of PPARα weakens the effect of sorafenib on MDSCs in mice with HCC. Pharmacological inhibition of PPARα has a synergistic anti-tumor effect with sorafenib, which is attenuated by the inhibition of MDSCs. Mechanistically, sorafenib significantly inhibited the differentiation of macrophages by upregulating PPARα expression and suppressing the PU.1-CSF1R pathway. Overall, our study demonstrated that sorafenib enhanced the function of MDSCs by facilitating PPARα-mediated FAO and further augmenting sorafenib resistance, which sheds light on dietary management and improves the therapeutic response in HCC.
{"title":"Sorafenib enhanced the function of myeloid-derived suppressor cells in hepatocellular carcinoma by facilitating PPARα-mediated fatty acid oxidation","authors":"Chunxiao Li, Liting Xiong, Yuhan Yang, Ping Jiang, Junjie Wang, Mengyuan Li, Shuhua Wei, Suqing Tian, Yuexuan Wang, Mi Zhang, Jie Tang","doi":"10.1186/s12943-025-02238-5","DOIUrl":"https://doi.org/10.1186/s12943-025-02238-5","url":null,"abstract":"Sorafenib, an FDA-approved drug for advanced hepatocellular carcinoma (HCC), faces resistance issues, partly due to myeloid-derived suppressor cells (MDSCs) that enhance immunosuppression in the tumor microenvironment (TME). Various murine HCC cell lines and MDSCs were used in a series of in vitro and in vivo experiments. These included subcutaneous tumor models, cell viability assays, flow cytometry, immunohistochemistry, and RNA sequencing. MDSCs were analyzed for chemotaxis, immunosuppressive functions, fatty acid oxidation (FAO), and PPARα expression. The impact of sorafenib on tumor growth, MDSC infiltration, differentiation, and immunosuppressive function was assessed, alongside the modulation of these processes by PPARα. Here, we revealed increased infiltration and enhanced function of MDSCs in TME after treatment with sorafenib. Moreover, our results indicated that sorafenib induced the accumulation of MDSCs mediated by CCR2, and pharmacological blockade of CCR2 markedly reduced MDSCs migration and tumor growth. Mechanistically, sorafenib promoted the effect and fatty acid uptake ability of MDSCs and modulated peroxisome proliferator-activated receptor α (PPARα)-mediated fatty acid oxidation (FAO). In addition, tumor-bearing mice fed a high-fat diet (HFD) at the beginning of sorafenib administration had worse outcomes than mice fed a regular diet. Genetic deficiency of PPARα weakens the effect of sorafenib on MDSCs in mice with HCC. Pharmacological inhibition of PPARα has a synergistic anti-tumor effect with sorafenib, which is attenuated by the inhibition of MDSCs. Mechanistically, sorafenib significantly inhibited the differentiation of macrophages by upregulating PPARα expression and suppressing the PU.1-CSF1R pathway. Overall, our study demonstrated that sorafenib enhanced the function of MDSCs by facilitating PPARα-mediated FAO and further augmenting sorafenib resistance, which sheds light on dietary management and improves the therapeutic response in HCC.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"45 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143050033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p><b>Correction</b><b>: </b><b>Mol Cancer 18, 174 (2019)</b></p><p><b>https://doi.org/10.1186/s12943-019-1105-0</b></p><br/><p>The authors identified two errors happened inadvertently in Figure 7 and Figure S5 after a self-investigation and carefully check of the original [1] published version.</p><p>The authors apologize for the error in Figure 7B. The annotations on the top of the last graph were wrongly typed. The annotations shall be “LDHA-low” and “LDHA-high”. The correct figure is shown below.</p><figure><picture><source srcset="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02229-6/MediaObjects/12943_2025_2229_Figa_HTML.png?as=webp" type="image/webp"/><img alt="figure a" aria-describedby="Figa" height="187" loading="lazy" src="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02229-6/MediaObjects/12943_2025_2229_Figa_HTML.png" width="685"/></picture></figure><p><b>Figure 7. Illustration of LINRIS-IGF2BP2-MYC axis in CRC. (B)</b> Percentages of specimens showing different levels of Ki-67, IGF2BP2, MYC, GLUT-1 and PKM2 and LDHA in the low or high LINRIS expression groups (n = 220, Chi-square test, **P < 0.01)</p><p>The authors also apologize for the error in Figure S5E. The ki-67 image of Ctrl was mistakenly uploaded. The correct figure is shown below.</p><figure><picture><source srcset="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02229-6/MediaObjects/12943_2025_2229_Figb_HTML.png?as=webp" type="image/webp"/><img alt="figure b" aria-describedby="Figb" height="511" loading="lazy" src="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02229-6/MediaObjects/12943_2025_2229_Figb_HTML.png" width="685"/></picture></figure><p><b>Figure S5. In vivo experiments elucidated the effect of the inhibition of LINRIS in CRC. (E)</b> Representative images of H&E staining, immunohistochemistry staining of Ki-67 and TUNEL from the tumor sections. Scale bar, 100 μm</p><ol data-track-component="outbound reference" data-track-context="references section"><li data-counter="1."><p>Wang Y, Lu JH, Wu QN, et al. LncRNA <i>LINRIS</i> stabilizes IGF2BP2 and promotes the aerobic glycolysis in colorectal cancer. Mol Cancer. 2019;18:174. https://doi.org/10.1186/s12943-019-1105-0.</p><p>Article PubMed PubMed Central CAS Google Scholar </p></li></ol><p>Download references<svg aria-hidden="true" focusable="false" height="16" role="img" width="16"><use xlink:href="#icon-eds-i-download-medium" xmlns:xlink="http://www.w3.org/1999/xlink"></use></svg></p><span>Author notes</span><ol><li><p>Yun Wang, Jia-Huan Lu, Qi-Nian Wu and Ying Jin contributed equally to this work.</p></li></ol><h3>Authors and Affiliations</h3><ol><li><p>State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China</p><p>Yun Wang, Jia-Huan Lu, Qi-Nian Wu, Ying Jin, De-Shen Wa
{"title":"Correction: LncRNA LINRIS stabilizes IGF2BP2 and promotes the aerobic glycolysis in colorectal cancer","authors":"Yun Wang, Jia-Huan Lu, Qi-Nian Wu, Ying Jin, De-Shen Wang, Yan-Xing Chen, Jia Liu, Xiao-Jing Luo, Qi Meng, Heng-Ying Pu, Ying-Nan Wang, Pei-Shan Hu, Ze-Xian Liu, Zhao-Lei Zeng, Qi Zhao, Rong Deng, Xiao-Feng Zhu, Huai-Qiang Ju, Rui-Hua Xu","doi":"10.1186/s12943-025-02229-6","DOIUrl":"https://doi.org/10.1186/s12943-025-02229-6","url":null,"abstract":"<p><b>Correction</b><b>: </b><b>Mol Cancer 18, 174 (2019)</b></p><p><b>https://doi.org/10.1186/s12943-019-1105-0</b></p><br/><p>The authors identified two errors happened inadvertently in Figure 7 and Figure S5 after a self-investigation and carefully check of the original [1] published version.</p><p>The authors apologize for the error in Figure 7B. The annotations on the top of the last graph were wrongly typed. The annotations shall be “LDHA-low” and “LDHA-high”. The correct figure is shown below.</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02229-6/MediaObjects/12943_2025_2229_Figa_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure a\" aria-describedby=\"Figa\" height=\"187\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02229-6/MediaObjects/12943_2025_2229_Figa_HTML.png\" width=\"685\"/></picture></figure><p><b>Figure 7. Illustration of LINRIS-IGF2BP2-MYC axis in CRC. (B)</b> Percentages of specimens showing different levels of Ki-67, IGF2BP2, MYC, GLUT-1 and PKM2 and LDHA in the low or high LINRIS expression groups (n = 220, Chi-square test, **P < 0.01)</p><p>The authors also apologize for the error in Figure S5E. The ki-67 image of Ctrl was mistakenly uploaded. The correct figure is shown below.</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02229-6/MediaObjects/12943_2025_2229_Figb_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure b\" aria-describedby=\"Figb\" height=\"511\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12943-025-02229-6/MediaObjects/12943_2025_2229_Figb_HTML.png\" width=\"685\"/></picture></figure><p><b>Figure S5. In vivo experiments elucidated the effect of the inhibition of LINRIS in CRC. (E)</b> Representative images of H&E staining, immunohistochemistry staining of Ki-67 and TUNEL from the tumor sections. Scale bar, 100 μm</p><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Wang Y, Lu JH, Wu QN, et al. LncRNA <i>LINRIS</i> stabilizes IGF2BP2 and promotes the aerobic glycolysis in colorectal cancer. Mol Cancer. 2019;18:174. https://doi.org/10.1186/s12943-019-1105-0.</p><p>Article PubMed PubMed Central CAS Google Scholar </p></li></ol><p>Download references<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></p><span>Author notes</span><ol><li><p>Yun Wang, Jia-Huan Lu, Qi-Nian Wu and Ying Jin contributed equally to this work.</p></li></ol><h3>Authors and Affiliations</h3><ol><li><p>State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, China</p><p>Yun Wang, Jia-Huan Lu, Qi-Nian Wu, Ying Jin, De-Shen Wa","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"4 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143044065","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The high mortality rate from hepatocellular carcinoma (HCC) is due primarily to challenges in early diagnosis and the development of drug resistance in advanced stages. Many first-line chemotherapeutic drugs induce ferroptosis, a form of programmed cell death dependent on ferrous iron-mediated oxidative stress, suggesting that drug resistance and ensuing tumor progression may in part stem from reduced ferroptosis. Since circular RNAs (circRNAs) have been shown to influence tumor development, we examined whether specific circRNAs may regulate drug-induced ferroptosis in HCC. Through circRNA sequencing, we identified a novel hsa_circ_0000195 (circTTC13) that is overexpressed in HCC tissues. This overexpression is linked to higher tumor grade, more advanced tumor stage, decreased ferroptosis, and poorer overall survival. Overexpression of CircTTC13 in HCC cell lines and explant tumors was associated with increased proliferation rates, enhanced metastatic capacity, and resistance to sorafenib, while also inhibiting ferroptosis. Conversely, circTTC13 silencing reduced malignant characteristics and promoted ferroptosis. In silico analysis, luciferase assays, and fluorescence in situ hybridization collectively demonstrated that circTTC13 directly targets and reduces miR-513a-5p expression, which in turn leads to the upregulation of the negative ferroptosis regulator SLC7A11. Moreover, the inhibition of SLC7A11 mirrored the effect of circTTC13 knockdown, whereas ferroptosis inhibition mimicked the effect of circTTC13 overexpression. Both circTTC13 and SLC7A11 were highly expressed in drug-resistant HCC cells, and circTTC13 silencing induced ferroptosis and reversed sorafenib resistance in explant tumors. These findings identify circTTC13 as a critical driver of HCC progression and resistance to drug-induced ferroptosis via upregulation of SLC7A11. The cicTTC13/miR-513a-5p/SLC7A11 axis represents a potential therapeutic target for HCC.
{"title":"CircTTC13 promotes sorafenib resistance in hepatocellular carcinoma through the inhibition of ferroptosis by targeting the miR-513a-5p/SLC7A11 axis","authors":"Ying Zhang, Ruiwei Yao, Mingyi Li, Chongkai Fang, Kunliang Feng, Xiuru Chen, Jinan Wang, Rui Luo, Hanqian Shi, Xinqiu Chen, Xilin Zhao, Hanlin Huang, Shuwei Liu, Bing Yin, Chong Zhong","doi":"10.1186/s12943-024-02224-3","DOIUrl":"https://doi.org/10.1186/s12943-024-02224-3","url":null,"abstract":"The high mortality rate from hepatocellular carcinoma (HCC) is due primarily to challenges in early diagnosis and the development of drug resistance in advanced stages. Many first-line chemotherapeutic drugs induce ferroptosis, a form of programmed cell death dependent on ferrous iron-mediated oxidative stress, suggesting that drug resistance and ensuing tumor progression may in part stem from reduced ferroptosis. Since circular RNAs (circRNAs) have been shown to influence tumor development, we examined whether specific circRNAs may regulate drug-induced ferroptosis in HCC. Through circRNA sequencing, we identified a novel hsa_circ_0000195 (circTTC13) that is overexpressed in HCC tissues. This overexpression is linked to higher tumor grade, more advanced tumor stage, decreased ferroptosis, and poorer overall survival. Overexpression of CircTTC13 in HCC cell lines and explant tumors was associated with increased proliferation rates, enhanced metastatic capacity, and resistance to sorafenib, while also inhibiting ferroptosis. Conversely, circTTC13 silencing reduced malignant characteristics and promoted ferroptosis. In silico analysis, luciferase assays, and fluorescence in situ hybridization collectively demonstrated that circTTC13 directly targets and reduces miR-513a-5p expression, which in turn leads to the upregulation of the negative ferroptosis regulator SLC7A11. Moreover, the inhibition of SLC7A11 mirrored the effect of circTTC13 knockdown, whereas ferroptosis inhibition mimicked the effect of circTTC13 overexpression. Both circTTC13 and SLC7A11 were highly expressed in drug-resistant HCC cells, and circTTC13 silencing induced ferroptosis and reversed sorafenib resistance in explant tumors. These findings identify circTTC13 as a critical driver of HCC progression and resistance to drug-induced ferroptosis via upregulation of SLC7A11. The cicTTC13/miR-513a-5p/SLC7A11 axis represents a potential therapeutic target for HCC.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"84 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143044103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-27DOI: 10.1186/s12943-025-02237-6
Zhikai Mai, Liwu Fu, Jiyan Su, Kenneth K.W. To, Chuansheng Yang, Chenglai Xia
<p><b>Correction: Mol Cancer 24</b>,<b> 6 (2025)</b></p><p><b>https://doi.org/10.1186/s12943-024-02202-9</b></p><p>Following the publication of the original article [1], the authors would like to update the texts under the Fig. 4 caption or legend.</p><p> The texts under the Fig. 4 caption currently reads:</p><p> Propionylcarnitine which was decreased by <i>S. multivorum</i> inhibits tumor growth <i>in vivo.</i> (<b>A</b>) Heatmap showing potential biomarker levels in mouse tumors. The screening criteria were <i>p</i> < 0.05 and |log2FC| ≥ 0 for unidimensional analysis, and VIP value > 1 for multidimensional analysis. (<b>B</b>) Pathway enrichment analysis of differential metabolites using pathway-associated metabolite sets (SMPDB). (<b>C</b>) Volcano plot showing the differential metabolites based on one-dimensional statistical screening. Differential metabolites were considered significant at a threshold of <i>p</i> < 0.05 and |log2FC| ≥ 0. (<b>D-F</b>) Concentration of short-chain acylcarnitine metabolites in mouse tumors. (<b>G</b>) The effect of propionylcarnitine on cell viability of MDA-MB-231, BT20, and 4T1 cell lines in vitro. (<b>H</b>) The effect of propionylcarnitine on spleen lymphocyte viability in BALB/c mice. (<b>I</b>) The number of Treg cells in splenic lymphocytes of BALB/c mice by flow cytometry analysis. (<b>L</b>) Images of representative 4T1 subcutaneous tumors after the intra-tumoral injection of the <i>S. multivorum</i> in BALB/c mice. PBS served as a negative control. 2 × 10<sup>7</sup> CFU of <i>S. multivorum</i> were injected into subcutaneous tumors as described above. 150 mg/kg propionylcarnitine was injected into the tumor twice a week. After 26 days, the subcutaneous tumors were isolated and shown. (<b>M</b>) Tumor growth curve in BALB/c mice. (<b>N</b>) Tumor weight in BALB/c mice. (<b>O</b>) Body weight of BALB/c mice. Statistical significance was determined by an unpaired two-tailed Student’s t-test for (<b>D-F</b>) and ANOVA statistical test with a Tukey’s post-hoc analysis for (<b>H</b>-<b>K</b>, <b>N</b>). Significance levels are denoted as *<i>p</i> < 0.05; **<i>p</i> < 0.01; ***<i>p</i> < 0.001.</p><p> The texts under the Fig. 4 caption should read:</p><p> Propionylcarnitine which was decreased by S. multivorum inhibits tumor growth in vivo. (<b>A</b>) Heatmap showing potential biomarker levels in mouse tumors. The screening criteria were <i>p</i> < 0.05 and |log2FC| ≥ 0 for unidimensional analysis, and VIP value > 1 for multidimensional analysis. (<b>B</b>) Pathway enrichment analysis of differential metabolites using pathway-associated metabolite sets (SMPDB). (<b>C</b>) Volcano plot showing the differential metabolites based on one-dimensional statistical screening. Differential metabolites were considered significant at a threshold of <i>p</i> < 0.05 and |log2FC| ≥ 0. (<b>D-F</b>) Concentration of short-chain acylcarnitine metabolites in mouse tumors. (<b>G</b>) The effect of
{"title":"Correction: Intra-tumoral sphingobacterium multivorum promotes triple-negative breast cancer progression by suppressing tumor immunosurveillance","authors":"Zhikai Mai, Liwu Fu, Jiyan Su, Kenneth K.W. To, Chuansheng Yang, Chenglai Xia","doi":"10.1186/s12943-025-02237-6","DOIUrl":"https://doi.org/10.1186/s12943-025-02237-6","url":null,"abstract":"<p><b>Correction: Mol Cancer 24</b>,<b> 6 (2025)</b></p><p><b>https://doi.org/10.1186/s12943-024-02202-9</b></p><p>Following the publication of the original article [1], the authors would like to update the texts under the Fig. 4 caption or legend.</p><p> The texts under the Fig. 4 caption currently reads:</p><p> Propionylcarnitine which was decreased by <i>S. multivorum</i> inhibits tumor growth <i>in vivo.</i> (<b>A</b>) Heatmap showing potential biomarker levels in mouse tumors. The screening criteria were <i>p</i> < 0.05 and |log2FC| ≥ 0 for unidimensional analysis, and VIP value > 1 for multidimensional analysis. (<b>B</b>) Pathway enrichment analysis of differential metabolites using pathway-associated metabolite sets (SMPDB). (<b>C</b>) Volcano plot showing the differential metabolites based on one-dimensional statistical screening. Differential metabolites were considered significant at a threshold of <i>p</i> < 0.05 and |log2FC| ≥ 0. (<b>D-F</b>) Concentration of short-chain acylcarnitine metabolites in mouse tumors. (<b>G</b>) The effect of propionylcarnitine on cell viability of MDA-MB-231, BT20, and 4T1 cell lines in vitro. (<b>H</b>) The effect of propionylcarnitine on spleen lymphocyte viability in BALB/c mice. (<b>I</b>) The number of Treg cells in splenic lymphocytes of BALB/c mice by flow cytometry analysis. (<b>L</b>) Images of representative 4T1 subcutaneous tumors after the intra-tumoral injection of the <i>S. multivorum</i> in BALB/c mice. PBS served as a negative control. 2 × 10<sup>7</sup> CFU of <i>S. multivorum</i> were injected into subcutaneous tumors as described above. 150 mg/kg propionylcarnitine was injected into the tumor twice a week. After 26 days, the subcutaneous tumors were isolated and shown. (<b>M</b>) Tumor growth curve in BALB/c mice. (<b>N</b>) Tumor weight in BALB/c mice. (<b>O</b>) Body weight of BALB/c mice. Statistical significance was determined by an unpaired two-tailed Student’s t-test for (<b>D-F</b>) and ANOVA statistical test with a Tukey’s post-hoc analysis for (<b>H</b>-<b>K</b>, <b>N</b>). Significance levels are denoted as *<i>p</i> < 0.05; **<i>p</i> < 0.01; ***<i>p</i> < 0.001.</p><p> The texts under the Fig. 4 caption should read:</p><p> Propionylcarnitine which was decreased by S. multivorum inhibits tumor growth in vivo. (<b>A</b>) Heatmap showing potential biomarker levels in mouse tumors. The screening criteria were <i>p</i> < 0.05 and |log2FC| ≥ 0 for unidimensional analysis, and VIP value > 1 for multidimensional analysis. (<b>B</b>) Pathway enrichment analysis of differential metabolites using pathway-associated metabolite sets (SMPDB). (<b>C</b>) Volcano plot showing the differential metabolites based on one-dimensional statistical screening. Differential metabolites were considered significant at a threshold of <i>p</i> < 0.05 and |log2FC| ≥ 0. (<b>D-F</b>) Concentration of short-chain acylcarnitine metabolites in mouse tumors. (<b>G</b>) The effect of ","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"113 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143044101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-24DOI: 10.1186/s12943-025-02230-z
Xiangying Deng, Yajun Gui, Lin Zhao
Microplastics, as an emerging environmental pollutant, have received widespread attention for their potential impact on ecosystems and human health. Microplastics are defined as plastic particles less than 5 millimeters in diameter and can be categorized as primary and secondary microplastics. Primary microplastics usually originate directly from industrial production, while secondary microplastics are formed by the degradation of larger plastic items. Microplastics are capable of triggering cytotoxicity and chronic inflammation, and may promote cancer through mechanisms such as pro-inflammatory responses, oxidative stress and endocrine disruption. In addition, improved microplastics bring new perspectives to cancer therapy, and studies of microplastics as drug carriers are underway, showing potential for high targeting and bioavailability. Although current studies suggest an association between microplastics and certain cancers (e.g., lung, liver, and breast cancers), the long-term effects and specific mechanisms still need to be studied. This review aimed at exploring the carcinogenicity of microplastics and their promising applications in cancer therapy provides important directions for future research and emphasizes the need for multidisciplinary collaboration to address this global health challenge.
{"title":"The micro(nano)plastics perspective: exploring cancer development and therapy","authors":"Xiangying Deng, Yajun Gui, Lin Zhao","doi":"10.1186/s12943-025-02230-z","DOIUrl":"https://doi.org/10.1186/s12943-025-02230-z","url":null,"abstract":"Microplastics, as an emerging environmental pollutant, have received widespread attention for their potential impact on ecosystems and human health. Microplastics are defined as plastic particles less than 5 millimeters in diameter and can be categorized as primary and secondary microplastics. Primary microplastics usually originate directly from industrial production, while secondary microplastics are formed by the degradation of larger plastic items. Microplastics are capable of triggering cytotoxicity and chronic inflammation, and may promote cancer through mechanisms such as pro-inflammatory responses, oxidative stress and endocrine disruption. In addition, improved microplastics bring new perspectives to cancer therapy, and studies of microplastics as drug carriers are underway, showing potential for high targeting and bioavailability. Although current studies suggest an association between microplastics and certain cancers (e.g., lung, liver, and breast cancers), the long-term effects and specific mechanisms still need to be studied. This review aimed at exploring the carcinogenicity of microplastics and their promising applications in cancer therapy provides important directions for future research and emphasizes the need for multidisciplinary collaboration to address this global health challenge.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"67 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143027198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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