Notably, clear cell renal cell carcinoma (ccRCC) is characterized by a distinct metabolic tumor phenotype that involves the reprogramming of multiple metabolic pathways. Although there is increasing evidence linking FUCA1 to malignancies, its specific role and downstream signaling pathways in ccRCC remain poorly understood. Here we found that FUCA1 expression was significantly downregulated in ccRCC tissues, which also predicts poor prognosis of ccRCCpatients. Moreover, enhancing FUCA1 expression resulted in reduced invasion and migration of ccRCC cells, further indicating its protective role. CHIP-qPCR and luciferase assays showed that CTCF was an upstream transcription factor of FUCA1 and could reverse the effects caused by FUCA1 inactivation. The change in FUCA1 led to changes in the results of various autophagy-related proteins and the mRFP-GFP-LC3 dual fluorescence system, indicating that it may play a role in the fusion stage of autophagy. Protein-protein interaction analysis revealed that FUCA2 exhibited the closest interaction with FUCA1 and strongly predicted the prognosis of ccRCC patients. Additionally, serum AFU encoded by FUCA2 could serve as a valuable predictor for survival in ccRCC patients. FUCA1 suppresses invasion and migration of ccRCC cells, with its activity being modulated by CTCF. FUCA1 regulates the autophagy process in ccRCC cells by influencing the fusion between autophagosomes and lysosomes. FUCA2 shares similarities with FUCA1, and elevated serum AFU levels along with increased expression of FUCA2 are indicative of a favorable prognosis in ccRCC.
{"title":"CTCF-activated FUCA1 functions as a tumor suppressor by promoting autophagy flux and serum α-L-fucosidase serves as a potential biomarker for prognosis in ccRCC.","authors":"Shuo Zhao, Jiajia Sun, Qinzheng Chang, Shuo Pang, Nianzhao Zhang, Yidong Fan, Jikai Liu","doi":"10.1186/s12935-024-03502-2","DOIUrl":"https://doi.org/10.1186/s12935-024-03502-2","url":null,"abstract":"<p><p>Notably, clear cell renal cell carcinoma (ccRCC) is characterized by a distinct metabolic tumor phenotype that involves the reprogramming of multiple metabolic pathways. Although there is increasing evidence linking FUCA1 to malignancies, its specific role and downstream signaling pathways in ccRCC remain poorly understood. Here we found that FUCA1 expression was significantly downregulated in ccRCC tissues, which also predicts poor prognosis of ccRCCpatients. Moreover, enhancing FUCA1 expression resulted in reduced invasion and migration of ccRCC cells, further indicating its protective role. CHIP-qPCR and luciferase assays showed that CTCF was an upstream transcription factor of FUCA1 and could reverse the effects caused by FUCA1 inactivation. The change in FUCA1 led to changes in the results of various autophagy-related proteins and the mRFP-GFP-LC3 dual fluorescence system, indicating that it may play a role in the fusion stage of autophagy. Protein-protein interaction analysis revealed that FUCA2 exhibited the closest interaction with FUCA1 and strongly predicted the prognosis of ccRCC patients. Additionally, serum AFU encoded by FUCA2 could serve as a valuable predictor for survival in ccRCC patients. FUCA1 suppresses invasion and migration of ccRCC cells, with its activity being modulated by CTCF. FUCA1 regulates the autophagy process in ccRCC cells by influencing the fusion between autophagosomes and lysosomes. FUCA2 shares similarities with FUCA1, and elevated serum AFU levels along with increased expression of FUCA2 are indicative of a favorable prognosis in ccRCC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"24 1","pages":"327"},"PeriodicalIF":5.3,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11439243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-27DOI: 10.1186/s12935-024-03506-y
Qing Li, Huixian Li, Ruiwen Zhu, William Chi Shing Cho, Xiaoqiang Yao, Fung Ping Leung, Gary Tse, Lai Kwok Leung, Wing Tak Wong
Breast cancer, the most prevalent and aggressive tumor affecting women, requires identification of disease determinants to facilitate the development of effective therapeutic strategies. Transient receptor potential vanilloid 2 (TRPV2), an ion channel highly permeable for calcium (Ca2+), is implicated in physiological and pathological processes. Nevertheless, the role of TRPV2 in breast cancer remains poorly elucidated. In this study, we found high levels of TRPV2 expression associated with advanced malignancy, thereby suggesting its potential as a biomarker for breast cancer staging. We demonstrated that TRPV2 activation promotes breast cancer cell proliferation, migration, and invasion, while silencing of TRPV2 suppresses breast cancer progression, highlighting the oncogenic role of TRPV2. Moreover, we reveal that TRPV2 facilitates cancer progression by modulating the CaMKKβ/AMPK/ULK1-autophagic axis through mediating calcium influx, providing new insights into TRPV2 as a novel therapeutic target for breast cancer treatment.
{"title":"TRPV2 calcium channel promotes breast cancer progression potential by activating autophagy.","authors":"Qing Li, Huixian Li, Ruiwen Zhu, William Chi Shing Cho, Xiaoqiang Yao, Fung Ping Leung, Gary Tse, Lai Kwok Leung, Wing Tak Wong","doi":"10.1186/s12935-024-03506-y","DOIUrl":"https://doi.org/10.1186/s12935-024-03506-y","url":null,"abstract":"<p><p>Breast cancer, the most prevalent and aggressive tumor affecting women, requires identification of disease determinants to facilitate the development of effective therapeutic strategies. Transient receptor potential vanilloid 2 (TRPV2), an ion channel highly permeable for calcium (Ca<sup>2+</sup>), is implicated in physiological and pathological processes. Nevertheless, the role of TRPV2 in breast cancer remains poorly elucidated. In this study, we found high levels of TRPV2 expression associated with advanced malignancy, thereby suggesting its potential as a biomarker for breast cancer staging. We demonstrated that TRPV2 activation promotes breast cancer cell proliferation, migration, and invasion, while silencing of TRPV2 suppresses breast cancer progression, highlighting the oncogenic role of TRPV2. Moreover, we reveal that TRPV2 facilitates cancer progression by modulating the CaMKKβ/AMPK/ULK1-autophagic axis through mediating calcium influx, providing new insights into TRPV2 as a novel therapeutic target for breast cancer treatment.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"24 1","pages":"324"},"PeriodicalIF":5.3,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11438410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-27DOI: 10.1186/s12935-024-03507-x
Liang Yang, Zhen Niu, Zhixuan Ma, Xiaojie Wu, Chi Teng Vong, Ge Li, Ying Feng
Gliomas are aggressive brain tumors associated with poor prognosis and limited treatment options due to their invasive nature and resistance to current therapeutic modalities. Research suggests that exosomal microRNAs have emerged as key players in intercellular communication within the tumor microenvironment, influencing tumor progression and therapeutic responses. Exosomal microRNAs (miRNAs), small non-coding RNAs, are crucial in glioma development, invasion, metastasis, angiogenesis, and immune evasion by binding to target genes. This comprehensive review examines the clinical relevance and implications of exosomal miRNAs in gliomas, highlighting their potential as diagnostic biomarkers, therapeutic targets and prognosis biomarker. Additionally, we also discuss the limitations of current exsomal miRNA treatments and address challenges and propose future directions for leveraging exosomal miRNAs in precision oncology for glioma management.
{"title":"Exploring the clinical implications and applications of exosomal miRNAs in gliomas: a comprehensive study.","authors":"Liang Yang, Zhen Niu, Zhixuan Ma, Xiaojie Wu, Chi Teng Vong, Ge Li, Ying Feng","doi":"10.1186/s12935-024-03507-x","DOIUrl":"https://doi.org/10.1186/s12935-024-03507-x","url":null,"abstract":"<p><p>Gliomas are aggressive brain tumors associated with poor prognosis and limited treatment options due to their invasive nature and resistance to current therapeutic modalities. Research suggests that exosomal microRNAs have emerged as key players in intercellular communication within the tumor microenvironment, influencing tumor progression and therapeutic responses. Exosomal microRNAs (miRNAs), small non-coding RNAs, are crucial in glioma development, invasion, metastasis, angiogenesis, and immune evasion by binding to target genes. This comprehensive review examines the clinical relevance and implications of exosomal miRNAs in gliomas, highlighting their potential as diagnostic biomarkers, therapeutic targets and prognosis biomarker. Additionally, we also discuss the limitations of current exsomal miRNA treatments and address challenges and propose future directions for leveraging exosomal miRNAs in precision oncology for glioma management.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"24 1","pages":"323"},"PeriodicalIF":5.3,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11437892/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-19DOI: 10.1186/s12935-024-03500-4
Chao Xu, Shuming Wang, Yong Sun
The aim of this study is to delve into the value of N6-Methyladenosine (m6A)-associated genes (MAGs) in pancreatic cancer (PC) prognosis. PC sequencing data and corresponding clinicopathological information were retrieved from GEO and TCGA databases. We filtered 19 MAGs in PC specimens and implemented functional annotation in biology. Later, the m6A modification pattern was stratified into m6Acluster A-B according to MAG expression levels, and further categorized into genecluster A-C based on differentially expressed genes between m6Acluster A and B. Next, a MAG-based prognostic prediction model was established by the least absolute shrinkage and selection operator (LASSO) regression analysis and multivariate Cox regression analysis. At last, the role of KRT7 in PC were explored. We found m6Acluster A pattern presented enrichment pathways associated with cell apoptosis, proliferation, migration, and cancer pathways. Additionally, high-risk group displayed more dismal prognosis and a higher programmed death-ligand 1 expression. The survival prediction ability of the model was verified in three independent PC GEO datasets. KRT7 is the most momentous risk gene in the established prognostic model. Among 18 clinical samples, the KRT7 protein in the surviving patient samples is lower than that in the deceased patient samples. We also identified elevated expression of KRT7 in PC tumor tissues compared to normal tissues using GEPIA 2. Then, the metastasis of PC cells was promoted by overexpressed KRT7 in vitro and in vivo. And IGF2BP3 upregulated KRT7 by increasing the mRNA stability of KRT7. The PPM built based on CXCL5, LY6K and KRT7 is an encouraging biomarker to define the prognosis. Additionally, IGF2BP3 promoted KRT7 by stabilizing mRNA of KRT7. And KRT7 promoted the metastasis of PC cells by promoting EMT.
本研究旨在探讨N6-甲基腺苷（m6A）相关基因（MAGs）在胰腺癌（PC）预后中的价值。我们从 GEO 和 TCGA 数据库中检索了 PC 测序数据和相应的临床病理信息。我们筛选了 PC 标本中的 19 个 MAGs，并在生物学中进行了功能注释。随后，根据MAG表达水平将m6A修饰模式分为m6A群A-B，并根据m6A群A和B之间的差异表达基因将其进一步分为基因群A-C。最后，研究人员探讨了 KRT7 在 PC 中的作用。我们发现，m6Acluster A模式呈现出与细胞凋亡、增殖、迁移和癌症通路相关的富集通路。此外，高危组的预后更差，程序性死亡配体 1 的表达更高。该模型的生存预测能力在三个独立的 PC GEO 数据集中得到了验证。在已建立的预后模型中，KRT7是最重要的风险基因。在18个临床样本中，存活患者样本中的KRT7蛋白低于死亡患者样本中的KRT7蛋白。我们还利用 GEPIA 2 发现，与正常组织相比，KRT7 在 PC 肿瘤组织中的表达升高。IGF2BP3通过增加KRT7的mRNA稳定性来上调KRT7。基于 CXCL5、LY6K 和 KRT7 建立的 PPM 是一种令人鼓舞的生物标志物，可用于确定预后。此外，IGF2BP3 通过稳定 KRT7 的 mRNA 来促进 KRT7。KRT7通过促进EMT促进了PC细胞的转移。
{"title":"The role of KRT7 in metastasis and prognosis of pancreatic cancer","authors":"Chao Xu, Shuming Wang, Yong Sun","doi":"10.1186/s12935-024-03500-4","DOIUrl":"https://doi.org/10.1186/s12935-024-03500-4","url":null,"abstract":"The aim of this study is to delve into the value of N6-Methyladenosine (m6A)-associated genes (MAGs) in pancreatic cancer (PC) prognosis. PC sequencing data and corresponding clinicopathological information were retrieved from GEO and TCGA databases. We filtered 19 MAGs in PC specimens and implemented functional annotation in biology. Later, the m6A modification pattern was stratified into m6Acluster A-B according to MAG expression levels, and further categorized into genecluster A-C based on differentially expressed genes between m6Acluster A and B. Next, a MAG-based prognostic prediction model was established by the least absolute shrinkage and selection operator (LASSO) regression analysis and multivariate Cox regression analysis. At last, the role of KRT7 in PC were explored. We found m6Acluster A pattern presented enrichment pathways associated with cell apoptosis, proliferation, migration, and cancer pathways. Additionally, high-risk group displayed more dismal prognosis and a higher programmed death-ligand 1 expression. The survival prediction ability of the model was verified in three independent PC GEO datasets. KRT7 is the most momentous risk gene in the established prognostic model. Among 18 clinical samples, the KRT7 protein in the surviving patient samples is lower than that in the deceased patient samples. We also identified elevated expression of KRT7 in PC tumor tissues compared to normal tissues using GEPIA 2. Then, the metastasis of PC cells was promoted by overexpressed KRT7 in vitro and in vivo. And IGF2BP3 upregulated KRT7 by increasing the mRNA stability of KRT7. The PPM built based on CXCL5, LY6K and KRT7 is an encouraging biomarker to define the prognosis. Additionally, IGF2BP3 promoted KRT7 by stabilizing mRNA of KRT7. And KRT7 promoted the metastasis of PC cells by promoting EMT.","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"13 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142264882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-19DOI: 10.1186/s12935-024-03504-0
Yuanxiang Chen, Shiyu Yang, Tao Yu, Tao Zeng, Lan Wei, Yiqing You, Jiafeng Tang, Tingting Dang, Haoli Sun, Yan Zhang
Recent studies have found that histone-modified genes play an increasingly important role in tumor progression. Lysine(K) specific demethylase 4A (KDM4A) is a histone lysine-specific demethylase highly expressed in a variety of malignant tumors, data showed that KDM4A was negatively correlated with the Bone Morphogenetic Protein 9 (BMP9) in breast cancer. And previous experiments have demonstrated that exogenous BMP9 significantly inhibits breast cancer development. We detected the expression of KDM4A in breast cancer and the relationship between KDM4A and BMP9 using real-time quantitative PCR (RT-qPCR) and Western blot, and verified the interaction between KDM4A and BMP9 by ChIP experiments. At the same time, we also detected whether KDM4A had effects on the RNA and protein stability of BMP9 using actinomycin D and cycloheximide. Measurement of alpha-ketoglutarate (α-KG) level by ELISA to observe the effect of BMP9 on glutamine metabolism in breast cancer cells. Nucleoplasmic distribution of KDM4A after exogenous BMP9 treatment in breast cancer cells were observed by immunofluorescence staining and Western blot. A subcutaneous xenograft tumor model in nude mice was used to study the therapeutic effects of exogenous BMP9 and KDM4A inhibitor (JIB-04) in breast cancer. CCK-8, conoly formation, Transwell, wound healing, and immunohistochemistry were used to monitor the growth of tumor and cell function. We found that KDM4A was abnormally highly expressed in breast cancer, and silenced BMP9 expression by removing histone methyl groups from the BMP9 gene region. Meanwhile, KDM4A could also reduce the stability of BMP9 protein. BMP9 inhibit glutamine metabolism in breast cancer, resulting in a decrease in its product α-KG, is confirmed by ELISA. Altered nucleoplasmic distribution of KDM4A due to decreased α-KG was confirmed by immunofluorescence staining and Western blot. Animal experiments confirm that the combination of exogenous BMP9 and JIB-04 shows significantly better results in breast cancer. KDM4A silences BMP9 expression by removing histone methyl groups from the BMP9 gene region, leading to further enhancement of glutamine metabolism, which contributes to malignant tumor progression. In addition, using JIB-04 in combination with exogenous BMP9 could inhibit the malignant progression of breast cancer cells and the growth of tumors more significantly.
{"title":"KDM4A promotes malignant progression of breast cancer by down-regulating BMP9 inducing consequent enhancement of glutamine metabolism","authors":"Yuanxiang Chen, Shiyu Yang, Tao Yu, Tao Zeng, Lan Wei, Yiqing You, Jiafeng Tang, Tingting Dang, Haoli Sun, Yan Zhang","doi":"10.1186/s12935-024-03504-0","DOIUrl":"https://doi.org/10.1186/s12935-024-03504-0","url":null,"abstract":"Recent studies have found that histone-modified genes play an increasingly important role in tumor progression. Lysine(K) specific demethylase 4A (KDM4A) is a histone lysine-specific demethylase highly expressed in a variety of malignant tumors, data showed that KDM4A was negatively correlated with the Bone Morphogenetic Protein 9 (BMP9) in breast cancer. And previous experiments have demonstrated that exogenous BMP9 significantly inhibits breast cancer development. We detected the expression of KDM4A in breast cancer and the relationship between KDM4A and BMP9 using real-time quantitative PCR (RT-qPCR) and Western blot, and verified the interaction between KDM4A and BMP9 by ChIP experiments. At the same time, we also detected whether KDM4A had effects on the RNA and protein stability of BMP9 using actinomycin D and cycloheximide. Measurement of alpha-ketoglutarate (α-KG) level by ELISA to observe the effect of BMP9 on glutamine metabolism in breast cancer cells. Nucleoplasmic distribution of KDM4A after exogenous BMP9 treatment in breast cancer cells were observed by immunofluorescence staining and Western blot. A subcutaneous xenograft tumor model in nude mice was used to study the therapeutic effects of exogenous BMP9 and KDM4A inhibitor (JIB-04) in breast cancer. CCK-8, conoly formation, Transwell, wound healing, and immunohistochemistry were used to monitor the growth of tumor and cell function. We found that KDM4A was abnormally highly expressed in breast cancer, and silenced BMP9 expression by removing histone methyl groups from the BMP9 gene region. Meanwhile, KDM4A could also reduce the stability of BMP9 protein. BMP9 inhibit glutamine metabolism in breast cancer, resulting in a decrease in its product α-KG, is confirmed by ELISA. Altered nucleoplasmic distribution of KDM4A due to decreased α-KG was confirmed by immunofluorescence staining and Western blot. Animal experiments confirm that the combination of exogenous BMP9 and JIB-04 shows significantly better results in breast cancer. KDM4A silences BMP9 expression by removing histone methyl groups from the BMP9 gene region, leading to further enhancement of glutamine metabolism, which contributes to malignant tumor progression. In addition, using JIB-04 in combination with exogenous BMP9 could inhibit the malignant progression of breast cancer cells and the growth of tumors more significantly.","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"16 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142264881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-18DOI: 10.1186/s12935-024-03501-3
Masoomeh Hosseini, Rana Ezzeddini, Seyed Mahmoud Hashemi, Sara Soudi, Amir Salek Farrokhi
Exosomes, membrane-enveloped vesicles found in various cell types, including Wharton’s jelly mesenchymal stem cells, play a crucial role in intercellular communication and regulation. Their use as a cell-free nanotechnology and drug delivery system has attracted attention. Triple-negative breast cancer (TNBC) is a major global health problem and is characterized by a high mortality rate. This study investigates the potential of Wharton’s Jelly mesenchymal stem cell-derived exosomes (WJ-Exo) as carriers of S3I-201 and their effects on STAT3 expression in breast cancer cell lines, and evaluates whether these exosomes can enhance the anti-tumor effect of S3I-201. The filtered WJ-Exos were analyzed by Transmission Electron Microscopy (TEM), Scanning electron microscopy (SEM), Dynamic Light Scattering (DLS), flow cytometry, and Western blotting. These exosomes were then used for loading with S3I-201, resulting in the nano-formulation WJ-Exo(S3I-201). The effect of WJ-Exo(S3I-201) on 4T1 cancer cells was investigated in vitro using MTT assay, flow cytometry, wound healing assay, Western blotting and Quantitative Real-Time Polymerase chain reaction (qPCR) analysis. Finally, the therapeutic efficacy of the nano-formulation was investigated in vivo using a tumor-bearing mouse model. In vitro experiments showed that co-incubation of 4T1 cells with the nano-formulation resulted in a significant reduction in p-STAT3 levels, induction of apoptosis, modulation of Bcl-2, Bax and caspase-3 protein and gene expression, and inhibition of migration. In vivo, treatment of tumor-bearing mice with WJ-Exo(S3I-201) showed a strong antitumor effect that exceeded the efficacy observed in the S3I-201 group. Our results demonstrate that WJ-Exo is an effective carrier for targeting S3I-201 to tumor cells and enhances the therapeutic efficacy of S3I-201 in tumor-bearing mice.
{"title":"Enhanced anti-tumor efficacy of S3I-201 in breast cancer mouse model through Wharton jelly- exosome","authors":"Masoomeh Hosseini, Rana Ezzeddini, Seyed Mahmoud Hashemi, Sara Soudi, Amir Salek Farrokhi","doi":"10.1186/s12935-024-03501-3","DOIUrl":"https://doi.org/10.1186/s12935-024-03501-3","url":null,"abstract":"Exosomes, membrane-enveloped vesicles found in various cell types, including Wharton’s jelly mesenchymal stem cells, play a crucial role in intercellular communication and regulation. Their use as a cell-free nanotechnology and drug delivery system has attracted attention. Triple-negative breast cancer (TNBC) is a major global health problem and is characterized by a high mortality rate. This study investigates the potential of Wharton’s Jelly mesenchymal stem cell-derived exosomes (WJ-Exo) as carriers of S3I-201 and their effects on STAT3 expression in breast cancer cell lines, and evaluates whether these exosomes can enhance the anti-tumor effect of S3I-201. The filtered WJ-Exos were analyzed by Transmission Electron Microscopy (TEM), Scanning electron microscopy (SEM), Dynamic Light Scattering (DLS), flow cytometry, and Western blotting. These exosomes were then used for loading with S3I-201, resulting in the nano-formulation WJ-Exo(S3I-201). The effect of WJ-Exo(S3I-201) on 4T1 cancer cells was investigated in vitro using MTT assay, flow cytometry, wound healing assay, Western blotting and Quantitative Real-Time Polymerase chain reaction (qPCR) analysis. Finally, the therapeutic efficacy of the nano-formulation was investigated in vivo using a tumor-bearing mouse model. In vitro experiments showed that co-incubation of 4T1 cells with the nano-formulation resulted in a significant reduction in p-STAT3 levels, induction of apoptosis, modulation of Bcl-2, Bax and caspase-3 protein and gene expression, and inhibition of migration. In vivo, treatment of tumor-bearing mice with WJ-Exo(S3I-201) showed a strong antitumor effect that exceeded the efficacy observed in the S3I-201 group. Our results demonstrate that WJ-Exo is an effective carrier for targeting S3I-201 to tumor cells and enhances the therapeutic efficacy of S3I-201 in tumor-bearing mice.","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"105 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142264889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-18DOI: 10.1186/s12935-024-03505-z
Guixin Wang, Cangchang Shi, Long He, Yingxi Li, Wenbin Song, Zhaohui Chen, Zhaoyi Liu, Yizeng Wang, Xianghui He, Yue Yu, Yao Tian, Xin Wang
Tumor metastasis is a continuous and dynamic process and is a major cause of tumor-related death in triple-negative breast cancer. However, this biological process remains largely unknown in triple-negative breast cancer. The emergence of single-cell sequencing enables a deeper understanding of the tumor microenvironment and provides a new strategy for discovering the potential mechanism of tumor metastasis. Herein, we integrated the single-cell expression profiling of primary and metastatic triple-negative breast cancer by Seurat package. Nine tumor cell subgroups were identified. Enrichment analysis suggested tumor subgroups (C0, C4) were associated with tumor metastasis with poor prognosis in TNBC. Weighted gene co-expression network was constructed and identified NENF was a metastasis-related gene. Subsequently, RT-qPCR, Immunohistochemistry, and western blot confirmed NENF is highly expressed in TNBC tissues. And cell function assays indicated NENF promote cell invasion and migration through regulating EMT in TNBC. Finally, TIDE and Connectivity Map database suggest the candidate drugs for targeting NENF. In conclusion, our findings provide a new insight into the progression and metastasis of TNBC and uncover NENF may be a prognostic biomarker and potential therapy targets.
{"title":"Identification of the tumor metastasis-related tumor subgroups overexpressed NENF in triple-negative breast cancer by single-cell transcriptomics","authors":"Guixin Wang, Cangchang Shi, Long He, Yingxi Li, Wenbin Song, Zhaohui Chen, Zhaoyi Liu, Yizeng Wang, Xianghui He, Yue Yu, Yao Tian, Xin Wang","doi":"10.1186/s12935-024-03505-z","DOIUrl":"https://doi.org/10.1186/s12935-024-03505-z","url":null,"abstract":"Tumor metastasis is a continuous and dynamic process and is a major cause of tumor-related death in triple-negative breast cancer. However, this biological process remains largely unknown in triple-negative breast cancer. The emergence of single-cell sequencing enables a deeper understanding of the tumor microenvironment and provides a new strategy for discovering the potential mechanism of tumor metastasis. Herein, we integrated the single-cell expression profiling of primary and metastatic triple-negative breast cancer by Seurat package. Nine tumor cell subgroups were identified. Enrichment analysis suggested tumor subgroups (C0, C4) were associated with tumor metastasis with poor prognosis in TNBC. Weighted gene co-expression network was constructed and identified NENF was a metastasis-related gene. Subsequently, RT-qPCR, Immunohistochemistry, and western blot confirmed NENF is highly expressed in TNBC tissues. And cell function assays indicated NENF promote cell invasion and migration through regulating EMT in TNBC. Finally, TIDE and Connectivity Map database suggest the candidate drugs for targeting NENF. In conclusion, our findings provide a new insight into the progression and metastasis of TNBC and uncover NENF may be a prognostic biomarker and potential therapy targets.","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"20 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142264884","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<p><b>Cancer Cell International (2020) 20:97</b></p><p><b>https://doi.org/10.1186/s12935-020-01186-y</b>.</p><p><b>Retraction Note</b></p><p>The Editor-in-Chief has retracted this article at the authors’ request. After publication, concerns were raised regarding the data included in the figures. Specifically:</p><ul> <li> <p>Fig. 1e 0 Gy images appear to be assembled incorrectly, and the EdU images for 0.125 and 0.25 µM S109 appear highly similar;</p> </li> <li> <p>Fig. 2c 0.25 µM 6 Gy image appears highly similar to Fig. 1i (C6 cells, 25 µM GDC-0449) of another article [1] from the same author group;</p> </li> <li> <p>Fig. 4b 0 mg/kg S109 10 Gy Day 10 (2nd mouse) and Day 18 (2nd mouse) images appear highly similar;</p> </li> <li> <p>Fig. 4e 0 mg/kg S109 10 Gy and 50 mg/kg S109 0 Gy images appear to overlap.</p> </li> </ul><p>The authors have stated that incorrect images were included in the figure panels during figure preparation. Although the authors believe that these issues do not affect the conclusions of the study, they requested to retract the article to prevent any potential confusion or misinterpretation by readers.</p><p>Xuejiao Liu stated on behalf of all authors that all authors agree to this retraction.</p><ol data-track-component="outbound reference" data-track-context="references section"><li data-counter="1."><p>Tu Y, Niu M, Xie P, et al. Smoothened is a poor prognosis factor and a potential therapeutic target in glioma. Sci Rep. 2017;7:42630. https://doi.org/10.1038/srep42630.</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>Insititute of Nervous System Diseases, Affiliated Hospital of Xuzhou Medical University, Xuzhou Medical University, Xuzhou, Jiangsu, China</p><p>Xuejiao Liu, Yiming Tu, Yifeng Wang, Di Zhou, Lin Shi, Guanzheng Liu, Xu Zhang, Huan Li, Shangfeng Gao, Mingshan Niu & Rutong Yu</p></li><li><p>Department of Neurosurgery, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China</p><p>Xuejiao Liu, Xu Zhang, Shangfeng Gao & Rutong Yu</p></li><li><p>Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China</p><p>Yiming Tu</p></li><li><p>Department of Neurosurgery, Suqian Hospital Affiliated to Xuzhou Medical University, Suqian, Jiangsu, China</p><p>Yulong Chong</p></li><li><p>College of Pharmacy, The Ohio State University, Columbus, OH, USA</p><p>Sijin Wu</p></li><li><p>Blood Diseases Institute, Xuzhou Medical University, Xuzhou, Jiangsu, China</p><p>Mingshan Niu</p></li></ol><span>Authors</span><ol><li><span>Xuejiao Liu</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Yiming Tu</span>View author publications<p>You can also search for this author
1186/s12935-024-03508-wDownload citationAccepted:13 September 2024Published: 18 September 2024DOI: https://doi.org/10.1186/s12935-024-03508-wShare this articleAnyone you share with the following link will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative
{"title":"Retraction Note: Reversible inhibitor of CRM1 sensitizes glioblastoma cells to radiation by blocking the NF-κB signaling pathway","authors":"Xuejiao Liu, Yiming Tu, Yifeng Wang, Di Zhou, Yulong Chong, Lin Shi, Guanzheng Liu, Xu Zhang, Sijin Wu, Huan Li, Shangfeng Gao, Mingshan Niu, Rutong Yu","doi":"10.1186/s12935-024-03508-w","DOIUrl":"https://doi.org/10.1186/s12935-024-03508-w","url":null,"abstract":"<p><b>Cancer Cell International (2020) 20:97</b></p><p><b>https://doi.org/10.1186/s12935-020-01186-y</b>.</p><p><b>Retraction Note</b></p><p>The Editor-in-Chief has retracted this article at the authors’ request. After publication, concerns were raised regarding the data included in the figures. Specifically:</p><ul>\u0000<li>\u0000<p>Fig. 1e 0 Gy images appear to be assembled incorrectly, and the EdU images for 0.125 and 0.25 µM S109 appear highly similar;</p>\u0000</li>\u0000<li>\u0000<p>Fig. 2c 0.25 µM 6 Gy image appears highly similar to Fig. 1i (C6 cells, 25 µM GDC-0449) of another article [1] from the same author group;</p>\u0000</li>\u0000<li>\u0000<p>Fig. 4b 0 mg/kg S109 10 Gy Day 10 (2nd mouse) and Day 18 (2nd mouse) images appear highly similar;</p>\u0000</li>\u0000<li>\u0000<p>Fig. 4e 0 mg/kg S109 10 Gy and 50 mg/kg S109 0 Gy images appear to overlap.</p>\u0000</li>\u0000</ul><p>The authors have stated that incorrect images were included in the figure panels during figure preparation. Although the authors believe that these issues do not affect the conclusions of the study, they requested to retract the article to prevent any potential confusion or misinterpretation by readers.</p><p>Xuejiao Liu stated on behalf of all authors that all authors agree to this retraction.</p><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Tu Y, Niu M, Xie P, et al. Smoothened is a poor prognosis factor and a potential therapeutic target in glioma. Sci Rep. 2017;7:42630. https://doi.org/10.1038/srep42630.</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>Insititute of Nervous System Diseases, Affiliated Hospital of Xuzhou Medical University, Xuzhou Medical University, Xuzhou, Jiangsu, China</p><p>Xuejiao Liu, Yiming Tu, Yifeng Wang, Di Zhou, Lin Shi, Guanzheng Liu, Xu Zhang, Huan Li, Shangfeng Gao, Mingshan Niu & Rutong Yu</p></li><li><p>Department of Neurosurgery, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China</p><p>Xuejiao Liu, Xu Zhang, Shangfeng Gao & Rutong Yu</p></li><li><p>Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China</p><p>Yiming Tu</p></li><li><p>Department of Neurosurgery, Suqian Hospital Affiliated to Xuzhou Medical University, Suqian, Jiangsu, China</p><p>Yulong Chong</p></li><li><p>College of Pharmacy, The Ohio State University, Columbus, OH, USA</p><p>Sijin Wu</p></li><li><p>Blood Diseases Institute, Xuzhou Medical University, Xuzhou, Jiangsu, China</p><p>Mingshan Niu</p></li></ol><span>Authors</span><ol><li><span>Xuejiao Liu</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Yiming Tu</span>View author publications<p>You can also search for this author ","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"1 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142264885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
<br/><p><b>Correction to: Cancer Cell International (2022) 22:32</b> <b>https://doi.org/10.1186/s12935-021-02434-5</b></p><br/><p>In this article [1], the WB band for mTOR in Fig. 3B and the Control group of T98G cells in Fig. 4A were incorrect. The corrected Figs. 3 and 4 are given below.</p><figure><figcaption><b data-test="figure-caption-text">Fig. 3</b></figcaption><picture><source srcset="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig3_HTML.png?as=webp" type="image/webp"/><img alt="figure 3" aria-describedby="Fig3" height="666" loading="lazy" src="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig3_HTML.png" width="685"/></picture><p>4, 5-Dimethoxycanthin-6-one inhibits the AKT/mTOR and MAPK signaling pathways. <b>A</b> 4, 5-Dimethoxycanthin-6-one inhibition of the AKT/mTOR and MAPK signaling pathways in U251 cells. <b>B</b> 4, 5-Dimethoxycanthin-6-one inhibition of the AKT/mTOR and MAPK signaling pathways in T98G cells. *P < 0.05 compared with the Control group</p><span>Full size image</span><svg aria-hidden="true" focusable="false" height="16" role="img" width="16"><use xlink:href="#icon-eds-i-chevron-right-small" xmlns:xlink="http://www.w3.org/1999/xlink"></use></svg></figure><figure><figcaption><b data-test="figure-caption-text">Fig. 4</b></figcaption><picture><source srcset="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig4_HTML.png?as=webp" type="image/webp"/><img alt="figure 4" aria-describedby="Fig4" height="1519" loading="lazy" src="//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig4_HTML.png" width="685"/></picture><p>4, 5-Dimethoxycanthin-6-one inhibits cell proliferation. <b>A</b> Cell proliferation detected using the EDU assay. <b>B</b> The migration distance of cells was measured using a wound scratch assay. <b>C</b> Colon numbers were analyzed using a colony formation assay. *P < 0.05 compared with the Control group</p><span>Full size image</span><svg aria-hidden="true" focusable="false" height="16" role="img" width="16"><use xlink:href="#icon-eds-i-chevron-right-small" xmlns:xlink="http://www.w3.org/1999/xlink"></use></svg></figure><ol data-track-component="outbound reference" data-track-context="references section"><li data-counter="1."><p>Li W, Huang BS, Xiong YY, Yang LJ, Wu LX. 4,5-Dimethoxycanthin-6-one is a novel LSD1 inhibitor that inhibits proliferation of glioblastoma cells and induces apoptosis and pyroptosis. Cancer Cell Int. 2022;22:32. https://doi.org/10.1186/s12935-021-02434-5.</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/
更正：Cancer Cell International (2022) 22:32 https://doi.org/10.1186/s12935-021-02434-5In 这篇文章[1]中，图 3B 中 mTOR 的 WB 波段和图 4A 中 T98G 细胞的对照组不正确。图 34，5-二甲氧基黄嘌呤-6-酮抑制 AKT/mTOR 和 MAPK 信号通路。A 4,5-二甲氧基黄嘌呤-6-酮抑制 U251 细胞中的 AKT/mTOR 和 MAPK 信号通路。B 4,5-二甲氧基黄嘌呤-6-酮对 T98G 细胞中 AKT/mTOR 和 MAPK 信号通路的抑制作用。*图 44，5-二甲氧基黄嘌呤-6-酮抑制细胞增殖。A 使用 EDU 检测法检测细胞增殖。B 用伤口划痕法测定细胞的迁移距离。C 利用集落形成试验分析集落数量。与对照组相比，*P < 0.05全图Li W, Huang BS, Xiong YY, Yang LJ, Wu LX.4,5-二甲氧基黄嘌呤-6-酮是一种新型 LSD1 抑制剂，可抑制胶质母细胞瘤细胞增殖并诱导细胞凋亡和热凋亡。Cancer Cell Int. 2022;22:32. https://doi.org/10.1186/s12935-021-02434-5.Article PubMed PubMed Central CAS Google Scholar Download references作者及单位湖南省长沙市湘雅路110号中南大学基础医学院生理学系李伟，黄柏生&；南昌大学第二附属医院神经外科，中国南昌 熊元元长沙市第一医院神经外科，中国长沙中国Li-Jian Yang作者Wei Li查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者Bai-Sheng Huang查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者Yuan-Yuan Xiong查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者Li-Jian Yang查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者Li-Xiang Wu查看作者发表的论文您也可以在PubMed Google Scholar中搜索该作者Corresponding authorCorrespondence to Li-Xiang Wu.开放获取 本文采用知识共享署名 4.0 国际许可协议进行许可，该协议允许以任何媒介或格式使用、共享、改编、分发和复制，只要您适当注明原作者和来源，提供知识共享许可协议的链接，并说明是否进行了修改。本文中的图片或其他第三方材料均包含在文章的知识共享许可协议中，除非在材料的署名栏中另有说明。如果材料未包含在文章的知识共享许可协议中，且您打算使用的材料不符合法律规定或超出许可使用范围，则您需要直接从版权所有者处获得许可。要查看该许可的副本，请访问 http://creativecommons.org/licenses/by/4.0/。除非在数据的信用行中另有说明，否则知识共享公共领域专用免责声明 (http://creativecommons.org/publicdomain/zero/1.0/) 适用于本文提供的数据。转载与许可引用本文Li, W., Huang, BS., Xiong, YY. et al. Correction：4,5-二甲氧基黄嘌呤-6-酮是一种新型 LSD1 抑制剂，可抑制胶质母细胞瘤细胞增殖并诱导细胞凋亡和热凋亡。Cancer Cell Int 24, 317 (2024). https://doi.org/10.1186/s12935-024-03311-7Download citationAccepted: 26 March 2024Published: 14 September 2024DOI: https://doi.org/10.1186/s12935-024-03311-7Share this articleAnyone you share the following link with will be able to read this content:Get shareable linkSorry, a shareable link is not currently available for this article.Copy to clipboard Provided by the Springer Nature SharedIt content-sharing initiative.
{"title":"Correction: 4,5-Dimethoxycanthin-6-one is a novel LSD1 inhibitor that inhibits proliferation of glioblastoma cells and induces apoptosis and pyroptosis","authors":"Wei Li, Bai-Sheng Huang, Yuan-Yuan Xiong, Li-Jian Yang, Li-Xiang Wu","doi":"10.1186/s12935-024-03311-7","DOIUrl":"https://doi.org/10.1186/s12935-024-03311-7","url":null,"abstract":"<br/><p><b>Correction to: Cancer Cell International (2022) 22:32</b> <b>https://doi.org/10.1186/s12935-021-02434-5</b></p><br/><p>In this article [1], the WB band for mTOR in Fig. 3B and the Control group of T98G cells in Fig. 4A were incorrect. The corrected Figs. 3 and 4 are given below.</p><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 3</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig3_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 3\" aria-describedby=\"Fig3\" height=\"666\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig3_HTML.png\" width=\"685\"/></picture><p>4, 5-Dimethoxycanthin-6-one inhibits the AKT/mTOR and MAPK signaling pathways. <b>A</b> 4, 5-Dimethoxycanthin-6-one inhibition of the AKT/mTOR and MAPK signaling pathways in U251 cells. <b>B</b> 4, 5-Dimethoxycanthin-6-one inhibition of the AKT/mTOR and MAPK signaling pathways in T98G cells. *P < 0.05 compared with the Control group</p><span>Full size image</span><svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></figure><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 4</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig4_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 4\" aria-describedby=\"Fig4\" height=\"1519\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs12935-024-03311-7/MediaObjects/12935_2024_3311_Fig4_HTML.png\" width=\"685\"/></picture><p>4, 5-Dimethoxycanthin-6-one inhibits cell proliferation. <b>A</b> Cell proliferation detected using the EDU assay. <b>B</b> The migration distance of cells was measured using a wound scratch assay. <b>C</b> Colon numbers were analyzed using a colony formation assay. *P < 0.05 compared with the Control group</p><span>Full size image</span><svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></figure><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Li W, Huang BS, Xiong YY, Yang LJ, Wu LX. 4,5-Dimethoxycanthin-6-one is a novel LSD1 inhibitor that inhibits proliferation of glioblastoma cells and induces apoptosis and pyroptosis. Cancer Cell Int. 2022;22:32. https://doi.org/10.1186/s12935-021-02434-5.</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/","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"34 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142269199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-13DOI: 10.1186/s12935-024-03499-8
Jun Rong, Qifu Wang, Tingzheng Li, Jin Qian, Jinchao Cheng
Glioma is a primary brain tumor that grows quickly, has an unfavorable prognosis, and can spread intracerebrally. Glioma cells rely on glucose as the major energy source, and glycolysis plays a critical role in tumorigenesis and progression. Substrate utilization shifts throughout glioma progression to facilitate energy generation and biomass accumulation. This metabolic reprogramming promotes glioma cell proliferation and metastasis and ultimately decreases the efficacy of conventional treatments. Non-coding RNAs (ncRNAs) are involved in several glucose metabolism pathways during tumor initiation and progression. These RNAs influence cell viability and glucose metabolism by modulating the expression of key genes of the glycolytic pathway. They can directly or indirectly affect glycolysis in glioma cells by influencing the transcription and post-transcriptional regulation of oncogenes and suppressor genes. In this review, we discussed the role of ncRNAs in the metabolic reprogramming of glioma cells and tumor microenvironments and their abnormal expression in the glucometabolic pathway in glioma. In addition, we consolidated the existing theoretical knowledge to facilitate the use of this emerging class of biomarkers as biological indicators and potential therapeutic targets for glioma.
{"title":"Glucose metabolism in glioma: an emerging sight with ncRNAs","authors":"Jun Rong, Qifu Wang, Tingzheng Li, Jin Qian, Jinchao Cheng","doi":"10.1186/s12935-024-03499-8","DOIUrl":"https://doi.org/10.1186/s12935-024-03499-8","url":null,"abstract":"Glioma is a primary brain tumor that grows quickly, has an unfavorable prognosis, and can spread intracerebrally. Glioma cells rely on glucose as the major energy source, and glycolysis plays a critical role in tumorigenesis and progression. Substrate utilization shifts throughout glioma progression to facilitate energy generation and biomass accumulation. This metabolic reprogramming promotes glioma cell proliferation and metastasis and ultimately decreases the efficacy of conventional treatments. Non-coding RNAs (ncRNAs) are involved in several glucose metabolism pathways during tumor initiation and progression. These RNAs influence cell viability and glucose metabolism by modulating the expression of key genes of the glycolytic pathway. They can directly or indirectly affect glycolysis in glioma cells by influencing the transcription and post-transcriptional regulation of oncogenes and suppressor genes. In this review, we discussed the role of ncRNAs in the metabolic reprogramming of glioma cells and tumor microenvironments and their abnormal expression in the glucometabolic pathway in glioma. In addition, we consolidated the existing theoretical knowledge to facilitate the use of this emerging class of biomarkers as biological indicators and potential therapeutic targets for glioma.","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"37 1","pages":""},"PeriodicalIF":5.8,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142203546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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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