Pub Date : 2025-06-01Epub Date: 2025-02-12DOI: 10.1016/j.adcanc.2025.100136
Wei Jin , Jue-jue Wang , Yan-fei Feng , Bing Chen, Zhao-hua Hu
5-Fluorouracil (5-FU) remains a cornerstone in colorectal cancer (CRC) chemotherapy; however, its clinical efficacy is often compromised by the development of resistance. Histone deacetylase 3 (HDAC3) has been implicated in chemoresistance across various cancers, yet its precise role in mediating 5-FU resistance in CRC remains poorly understood. In this study, we established a 5-FU-resistant CRC cell line (HCT116/5-FU) by gradually exposing parental HCT116 cells to increasing 5-FU concentrations. Screening of HDAC family members revealed significant upregulation of HDAC3 at both mRNA and protein levels in resistant cells. Mechanistically, we show that HDAC3 promotes 5-FU resistance by destabilizing the cyclin-dependent kinase inhibitor p21 through deacetylation, enhancing its ubiquitination and subsequent degradation. This HDAC3-mediated reduction in p21 levels disrupts cell cycle control, contributing to chemoresistance. Importantly, treatment with the HDAC3-specific inhibitor RGFP966 restored p21 stability, reduced colony formation, and sensitized HCT116/5-FU cells to 5-FU. Xenograft experiments further validated the synergistic efficacy of RGFP966 and 5-FU in vivo. These findings identify HDAC3 as a critical regulator of 5-FU resistance through modulation of p21 stability and suggest that combining HDAC3 inhibitors with conventional chemotherapy represents a promising strategy to overcome chemoresistance in CRC patients.
{"title":"HDAC3-mediated deacetylation of p21 stabilizes protein levels and promotes 5-FU resistance in colorectal cancer cells","authors":"Wei Jin , Jue-jue Wang , Yan-fei Feng , Bing Chen, Zhao-hua Hu","doi":"10.1016/j.adcanc.2025.100136","DOIUrl":"10.1016/j.adcanc.2025.100136","url":null,"abstract":"<div><div>5-Fluorouracil (5-FU) remains a cornerstone in colorectal cancer (CRC) chemotherapy; however, its clinical efficacy is often compromised by the development of resistance. Histone deacetylase 3 (HDAC3) has been implicated in chemoresistance across various cancers, yet its precise role in mediating 5-FU resistance in CRC remains poorly understood. In this study, we established a 5-FU-resistant CRC cell line (HCT116/5-FU) by gradually exposing parental HCT116 cells to increasing 5-FU concentrations. Screening of HDAC family members revealed significant upregulation of HDAC3 at both mRNA and protein levels in resistant cells. Mechanistically, we show that HDAC3 promotes 5-FU resistance by destabilizing the cyclin-dependent kinase inhibitor p21 through deacetylation, enhancing its ubiquitination and subsequent degradation. This HDAC3-mediated reduction in p21 levels disrupts cell cycle control, contributing to chemoresistance. Importantly, treatment with the HDAC3-specific inhibitor RGFP966 restored p21 stability, reduced colony formation, and sensitized HCT116/5-FU cells to 5-FU. Xenograft experiments further validated the synergistic efficacy of RGFP966 and 5-FU in vivo. These findings identify HDAC3 as a critical regulator of 5-FU resistance through modulation of p21 stability and suggest that combining HDAC3 inhibitors with conventional chemotherapy represents a promising strategy to overcome chemoresistance in CRC patients.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"14 ","pages":"Article 100136"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-06-01Epub Date: 2025-02-07DOI: 10.1016/j.adcanc.2025.100134
Asma Jan, Shazia Sofi, Manzoor Ahmad Mir
Background
Breast cancer is the second top mortality of women globally. A major difficulty in therapeutic therapy is the disease's heterogeneity. However, modern discoveries in molecular biology and immunology have made it possible to create highly focused medicines for a variety of breast tumor subtypes. The fundamental aim of targeted treatments is to inhibit the growth of tumors by blocking the activity of a particular target or molecule. Morphological alterations in neuronal-glial cells have been linked to breast cancer (BC) on several occasions. However, the processes by which these neuronal proteins are regulated remain unclear despite their association with cancer. Analysis of the expression of genes in tissues of human BC has recognized microtubule-binding protein Tau to be a newly identified marker of response to paclitaxel and a modulator of paclitaxel sensitivity. In terms of taxane resistance pathways, those involving MAPs (microtubule-associated proteins) such as Tau are crucial. Reduced concentration of the Tau protein makes the microtubules of the mitochondrion and the cytoskeleton more vulnerable to the effects of the drug paclitaxel, which can disrupt mitosis and interfere with cell signalling. Clinical and preclinical data from the past several years support the hypothesis that ER induces the gene MAP-Tau and the resulting expression of the Tau protein influences the susceptibility of malignant cells to taxanes.
Aim
This study illustrates the expression pattern and prognostic significance of MAPT (Microtubule-Associated Proteins Tau) in BC and targeting MAPT using Paclitaxel drug.
Methods
The present study employed both In Silico and In Vitro methodologies to evaluate the expression profile, prognostic, and therapeutic value of the MAPT gene in BC and discover the interactions of MAPT in breast cancer pathogenesis.
Results
The In-Silico and In-Vitro studies have also revealed that patients with BC will have much better therapeutic responses when MAPT is inhibited in addition to normal therapies because overexpression of MAPT promotes tumor formation.
Conclusion
Overall, our research indicates that MAPT is associated with tumor growth in BC cells and its dysregulation has been implicated in breast cancer pathogenesis.
背景乳腺癌是全球女性死亡率第二高的疾病。这种疾病的异质性是治疗的一大难题。然而，现代分子生物学和免疫学的发现使得针对各种乳腺肿瘤亚型的高针对性药物成为可能。靶向治疗的根本目的是通过阻断特定靶点或分子的活性来抑制肿瘤的生长。神经元-胶质细胞的形态改变多次与乳腺癌（BC）有关。然而，尽管这些神经元蛋白与癌症有关，但其调节过程仍不清楚。对人类 BC 组织中基因表达的分析发现，微管结合蛋白 Tau 是新发现的紫杉醇反应标志物，也是紫杉醇敏感性的调节因子。就紫杉醇抗性途径而言，涉及 Tau 等微管相关蛋白（MAPs）的途径至关重要。Tau 蛋白浓度降低会使线粒体的微管和细胞骨架更容易受到紫杉醇药物的影响，从而破坏有丝分裂并干扰细胞信号。过去几年的临床和临床前数据支持ER诱导基因MAP-Tau，由此导致的Tau蛋白表达影响恶性细胞对紫杉类药物的易感性这一假设。方法本研究采用了体内和体外方法来评估 MAPT 基因在乳腺癌中的表达谱、预后和治疗价值，并发现 MAPT 在乳腺癌发病机制中的相互作用。结论总之，我们的研究表明，MAPT 与 BC 细胞中肿瘤的生长有关，它的失调与乳腺癌的发病机制有关。
{"title":"Unravelling the oncogenic potential and prognostic significance of MAPT in breast cancer: An In-Silico inhibition of MAPT by paclitaxel","authors":"Asma Jan, Shazia Sofi, Manzoor Ahmad Mir","doi":"10.1016/j.adcanc.2025.100134","DOIUrl":"10.1016/j.adcanc.2025.100134","url":null,"abstract":"<div><h3>Background</h3><div>Breast cancer is the second top mortality of women globally. A major difficulty in therapeutic therapy is the disease's heterogeneity. However, modern discoveries in molecular biology and immunology have made it possible to create highly focused medicines for a variety of breast tumor subtypes. The fundamental aim of targeted treatments is to inhibit the growth of tumors by blocking the activity of a particular target or molecule. Morphological alterations in neuronal-glial cells have been linked to breast cancer (BC) on several occasions. However, the processes by which these neuronal proteins are regulated remain unclear despite their association with cancer. Analysis of the expression of genes in tissues of human BC has recognized microtubule-binding protein Tau to be a newly identified marker of response to paclitaxel and a modulator of paclitaxel sensitivity. In terms of taxane resistance pathways, those involving MAPs (microtubule-associated proteins) such as Tau are crucial. Reduced concentration of the Tau protein makes the microtubules of the mitochondrion and the cytoskeleton more vulnerable to the effects of the drug paclitaxel, which can disrupt mitosis and interfere with cell signalling. Clinical and preclinical data from the past several years support the hypothesis that ER induces the gene MAP-Tau and the resulting expression of the Tau protein influences the susceptibility of malignant cells to taxanes.</div></div><div><h3>Aim</h3><div>This study illustrates the expression pattern and prognostic significance of MAPT (Microtubule-Associated Proteins Tau) in BC and targeting MAPT using Paclitaxel drug.</div></div><div><h3>Methods</h3><div>The present study employed both <strong><em>In Silico</em></strong> and <strong><em>In Vitro</em></strong> methodologies to evaluate the expression profile, prognostic, and therapeutic value of the MAPT gene in BC and discover the interactions of MAPT in breast cancer pathogenesis.</div></div><div><h3>Results</h3><div>The <strong><em>In-Silico</em></strong> and <strong><em>In-Vitro</em></strong> studies have also revealed that patients with BC will have much better therapeutic responses when MAPT is inhibited in addition to normal therapies because overexpression of MAPT promotes tumor formation.</div></div><div><h3>Conclusion</h3><div>Overall, our research indicates that MAPT is associated with tumor growth in BC cells and its dysregulation has been implicated in breast cancer pathogenesis.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"14 ","pages":"Article 100134"},"PeriodicalIF":2.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143643580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Castration-resistant prostate cancer (CRPC) is the severe and metastatic form of prostate cancer and demands effective, reliable diagnostic and therapeutic approaches. It has been shown that long non-coding RNAs (lncRNAs) dysregulations promote metastasis in tumors. The current research aim is to identify dysregulated lncRNAs in metastatic CRPC.
Materials and methods
R programs along with multiple packages were applied to identify novel lncRNAs dysregulated in CRPC. Raw data of clinical samples were obtained from NCBI-GSE74685, which consisted of metastatic and non-metastatic CRPC samples, and was analyzed through a limma package of R with defined cutoff criteria as adjusted P-value < 0.05 and |Fold Change = FC| ≥ ±1. To further understand lncRNA co-expression gene modules, WGCNA analysis, hub-gene identification, and pathway enrichment were performed.
Results
Four dysregulated lncRNAs were identified with more than a two-fold change in expression levels, including TP53TG1, RFPL1S, DLEU1, and HCG4. WGCNA analysis results in royal blue, salmon, light cyan, and blue co-expression modules with dysregulated lncRNAs. According to a pathway enrichment study, these co-expressed modules showed enrichment in highly relevant pathways to the CRPC metastatic process, including mesenchymal-to-epithelial transition, purine metabolism, C-MYB transcription factor network, and immune system. In addition, SOD2, PRKCA, IL6, and ITGAM were identified as hub genes.
Conclusion
The current study suggests dysregulation of TP53TG1, RFPL1S, DLEU1, and HCG4 lncRNAs and corresponding hub genes may promote CRPC metastasis through the EMT pathways.
{"title":"Dysregulated key long non-coding RNAs TP53TG1, RFPL1S, DLEU1, and HCG4 associated with epithelial-mesenchymal transition (EMT) in castration-resistant prostate cancer","authors":"Tahmineh Mehrabi , Roozbeh Heidarzadehpilehrood , Meysam Mobasheri , Tabassom Sobati , Masoumeh Heshmati , Maryam Pirhoushiaran","doi":"10.1016/j.adcanc.2025.100132","DOIUrl":"10.1016/j.adcanc.2025.100132","url":null,"abstract":"<div><h3>Background</h3><div>Castration-resistant prostate cancer (CRPC) is the severe and metastatic form of prostate cancer and demands effective, reliable diagnostic and therapeutic approaches. It has been shown that long non-coding RNAs (lncRNAs) dysregulations promote metastasis in tumors. The current research aim is to identify dysregulated lncRNAs in metastatic CRPC.</div></div><div><h3>Materials and methods</h3><div>R programs along with multiple packages were applied to identify novel lncRNAs dysregulated in CRPC. Raw data of clinical samples were obtained from NCBI-GSE74685, which consisted of metastatic and non-metastatic CRPC samples, and was analyzed through a limma package of R with defined cutoff criteria as adjusted <em>P-value</em> < 0.05 and |Fold Change = FC| ≥ ±1. To further understand lncRNA co-expression gene modules, WGCNA analysis, hub-gene identification, and pathway enrichment were performed.</div></div><div><h3>Results</h3><div>Four dysregulated lncRNAs were identified with more than a two-fold change in expression levels, including TP53TG1, RFPL1S, DLEU1, and HCG4. WGCNA analysis results in royal blue, salmon, light cyan, and blue co-expression modules with dysregulated lncRNAs. According to a pathway enrichment study, these co-expressed modules showed enrichment in highly relevant pathways to the CRPC metastatic process, including mesenchymal-to-epithelial transition, purine metabolism, C-MYB transcription factor network, and immune system. In addition, SOD2, PRKCA, IL6, and ITGAM were identified as hub genes.</div></div><div><h3>Conclusion</h3><div>The current study suggests dysregulation of TP53TG1, RFPL1S, DLEU1, and HCG4 lncRNAs and corresponding hub genes may promote CRPC metastasis through the EMT pathways.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"13 ","pages":"Article 100132"},"PeriodicalIF":2.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143151537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01Epub Date: 2025-02-26DOI: 10.1016/j.adcanc.2025.100137
Sonam Agarwal, Anita Chauhan, Pramod Kumar Gautam
This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/policies/article-withdrawal).
This article has been retracted at the request of the Editor-in-Chief.
Concern was raised about validity and reliability of the data, experimental procedures, data analysis methods and consequently the result of the article.
The Editors requested the corresponding author to repeat the experiments at least three times and provide the raw data and standard deviations for the statistically evaluated results. However, the authors did not follow the Editors' recommendations and were unable to provide adequate response for comment. The overall validity of the results could not be confirmed. Therefore, the Editor-in-Chief decided to retract the article.
{"title":"Retraction notice to “Immunomodulatory effects of β-defensin 2 on tumor associated macrophages induced antitumor function in breast cancer” [Adv. Cancer Biol. – Metastasis 7 (2023) 100102]","authors":"Sonam Agarwal, Anita Chauhan, Pramod Kumar Gautam","doi":"10.1016/j.adcanc.2025.100137","DOIUrl":"10.1016/j.adcanc.2025.100137","url":null,"abstract":"<div><div>This article has been retracted: please see Elsevier Policy on Article Withdrawal (<span><span>https://www.elsevier.com/about/policies/article-withdrawal</span><svg><path></path></svg></span>).</div><div>This article has been retracted at the request of the Editor-in-Chief.</div><div>Concern was raised about validity and reliability of the data, experimental procedures, data analysis methods and consequently the result of the article.</div><div>The Editors requested the corresponding author to repeat the experiments at least three times and provide the raw data and standard deviations for the statistically evaluated results. However, the authors did not follow the Editors' recommendations and were unable to provide adequate response for comment. The overall validity of the results could not be confirmed. Therefore, the Editor-in-Chief decided to retract the article.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"13 ","pages":"Article 100137"},"PeriodicalIF":2.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143610692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01Epub Date: 2025-02-16DOI: 10.1016/j.adcanc.2025.100135
Jie Li , Yehan Zhu
Objective
Non-small lung cancer (NSCLC) is the most prevalent form of lung cancer, and it is often associated with poor patient outcomes. Erythropoietin-producing hepatocellular receptor A5 (EPHA5), a member of the Eph tyrosine kinase receptor family, has been implicated in various stages of tumor progression. However, the specific role of EPHA5 in NSCLC remains poorly understood. This study aims to explore the influence of EPHA5 on the stemness of NSCLC cancer cells and their sensitivity to gefitinib, while also investigating the underlying mechanisms involved.
Methods
EPHA5 expression was suppressed using small interfering ribonucleic acids (siRNAs), while qPCR and Western blot were applied to analyze the knockdown efficiency. Subsequently, the expressions of stem cell-related markers, such as SOX2, Nanog, KLF4, Oct4, and β-catenin, were detected and quantified via qPCR and Western blot during the experiment, while CD133-positive cells were analyzed via flow cytometry. Gefitinib sensitivity was evaluated in EPHA5-knockdown cells. The Wnt activator, CHIR-99021, was employed to rescue β-catenin expression.
Results
EPHA5 expression was elevated in NSCLC cell lines (NCI-H460 and NCI-H1229) but considerably downregulated by siRNAs. EPHA5 knockdown alleviated stemness, enhanced gefitinib sensitivity, and suppressed Wnt activation, as evidenced by lower CD133-positive cells, and decreased expression of Sox2, Nanog, KLF4, Oct4, and β-catenin. The Wnt activator reversed the inhibitory effect of EPHA5 on cancer cell stemness by upregulating β-catenin.
Conclusion
Silencing the expression of EPHA5 can reduce NSCLC stemness and enhance gefitinib sensitivity by inhibiting the Wnt signaling pathway.
Strengths and limitations of this study
We find EPHA5 enhances stemness and decreases gefitinib sensitivity via Wnt signaling pathway of non-small cell lung cancer but prognostic follow-up of lung adenocarcinoma patients in this study is lacking.
{"title":"EPHA5 enhances stemness and decreases gefitinib sensitivity via Wnt signaling pathway in non-small lung cancer","authors":"Jie Li , Yehan Zhu","doi":"10.1016/j.adcanc.2025.100135","DOIUrl":"10.1016/j.adcanc.2025.100135","url":null,"abstract":"<div><h3>Objective</h3><div>Non-small lung cancer (NSCLC) is the most prevalent form of lung cancer, and it is often associated with poor patient outcomes. Erythropoietin-producing hepatocellular receptor A5 (EPHA5), a member of the Eph tyrosine kinase receptor family, has been implicated in various stages of tumor progression. However, the specific role of EPHA5 in NSCLC remains poorly understood. This study aims to explore the influence of EPHA5 on the stemness of NSCLC cancer cells and their sensitivity to gefitinib, while also investigating the underlying mechanisms involved.</div></div><div><h3>Methods</h3><div>EPHA5 expression was suppressed using small interfering ribonucleic acids (siRNAs), while qPCR and Western blot were applied to analyze the knockdown efficiency. Subsequently, the expressions of stem cell-related markers, such as SOX2, Nanog, KLF4, Oct4, and β-catenin, were detected and quantified via qPCR and Western blot during the experiment, while CD133-positive cells were analyzed via flow cytometry. Gefitinib sensitivity was evaluated in EPHA5-knockdown cells. The Wnt activator, CHIR-99021, was employed to rescue β-catenin expression.</div></div><div><h3>Results</h3><div>EPHA5 expression was elevated in NSCLC cell lines (NCI-H460 and NCI-H1229) but considerably downregulated by siRNAs. EPHA5 knockdown alleviated stemness, enhanced gefitinib sensitivity, and suppressed Wnt activation, as evidenced by lower CD133-positive cells, and decreased expression of Sox2, Nanog, KLF4, Oct4, and β-catenin. The Wnt activator reversed the inhibitory effect of EPHA5 on cancer cell stemness by upregulating β-catenin.</div></div><div><h3>Conclusion</h3><div>Silencing the expression of EPHA5 can reduce NSCLC stemness and enhance gefitinib sensitivity by inhibiting the Wnt signaling pathway.</div></div><div><h3>Strengths and limitations of this study</h3><div>We find EPHA5 enhances stemness and decreases gefitinib sensitivity via Wnt signaling pathway of non-small cell lung cancer but prognostic follow-up of lung adenocarcinoma patients in this study is lacking.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"13 ","pages":"Article 100135"},"PeriodicalIF":2.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143474318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01Epub Date: 2024-11-26DOI: 10.1016/j.adcanc.2024.100131
Valentin Baumgartner , Thomas Paul Scherer , Ashkan Mortezavi , Niels Rupp , Holger Moch , Peter Wild , Susanne Dettwiler , Miriam Wanner , Dominik Enderlin , Souzan Salemi , Daniel Eberli
Background
The mitochondrial metabolism in prostate cancer (PCa) is of great importance due the unique metabolic shift from glycolysis to oxidative phosphorylation. In this study, we aimed to analyze the expression level of mitochondrial markers TOM20, DRP1 and OPA1 in benign and malignant tissue, to assess if these markers are associated with different grade and stage of PCa.
Materials and methods
This study assessed TOM20, DRP1, and OPA1 expression in formalin-fixed, paraffin-embedded prostate tissue samples, including benign and malignant tissue specimen. Immunohistochemistry on tissue microarrays was conducted, with staining intensities scored semi-quantitatively. Statistical analyses evaluated associations with PCa grade and stage. A survival analysis for biochemical recurrence (RFS), overall survival (OS) and disease specific survival (DSS) was performed using multivariate Cox regression analysis to assess prognostic properties of the markers.
Results
In total, 527 patients were included in our analysis, which composed of 45 (8.5 %) benign prostate hyperplasia (BPH) and 482 (91.5 %) PCa samples (436 localized (90.5 %) and 46 (9.5 %) metastatic). Immunoreactivity for TOM20, DRP1 and OPA1 was strong in 2 of 43 (4.7 %), 1 of 43 (2.3 %) and 0 of 43 (0 %) of BPH control tissue. Strong marker expression was significantly increased in radical prostatectomy specimen (TOM20: 111/371 (29.9 %), DRP1: 89/373 (23.9 %), OPA1: 60/371 (16.2 %), p < 0.001) and in metastatic tissue (TOM20: 22/42 (52.4 %), DRP1: 14/42 (33.3 %), OPA1: 21/41 (51.2 %), p < 0.001). None of the markers demonstrated prognostic properties for RFS, OS, and DSS.
Conclusion
A strong association between the expression of the mitochondrial markers TOM20, DRP1 and OPA1 and PCa aggressiveness was demonstrated. However, these markers were not found to be prognostic regarding RFS, OS and DSS. Future studies are needed focusing on the underlying mechanisms of the upregulation of mitochondrial metabolism in aggressive PCa and evaluate potential therapeutic implications.
{"title":"Upregulation of mitochondrial function is associated with advanced prostate cancer","authors":"Valentin Baumgartner , Thomas Paul Scherer , Ashkan Mortezavi , Niels Rupp , Holger Moch , Peter Wild , Susanne Dettwiler , Miriam Wanner , Dominik Enderlin , Souzan Salemi , Daniel Eberli","doi":"10.1016/j.adcanc.2024.100131","DOIUrl":"10.1016/j.adcanc.2024.100131","url":null,"abstract":"<div><h3>Background</h3><div>The mitochondrial metabolism in prostate cancer (PCa) is of great importance due the unique metabolic shift from glycolysis to oxidative phosphorylation. In this study, we aimed to analyze the expression level of mitochondrial markers TOM20, DRP1 and OPA1 in benign and malignant tissue, to assess if these markers are associated with different grade and stage of PCa.</div></div><div><h3>Materials and methods</h3><div>This study assessed TOM20, DRP1, and OPA1 expression in formalin-fixed, paraffin-embedded prostate tissue samples, including benign and malignant tissue specimen. Immunohistochemistry on tissue microarrays was conducted, with staining intensities scored semi-quantitatively. Statistical analyses evaluated associations with PCa grade and stage. A survival analysis for biochemical recurrence (RFS), overall survival (OS) and disease specific survival (DSS) was performed using multivariate Cox regression analysis to assess prognostic properties of the markers.</div></div><div><h3>Results</h3><div>In total, 527 patients were included in our analysis, which composed of 45 (8.5 %) benign prostate hyperplasia (BPH) and 482 (91.5 %) PCa samples (436 localized (90.5 %) and 46 (9.5 %) metastatic). Immunoreactivity for TOM20, DRP1 and OPA1 was strong in 2 of 43 (4.7 %), 1 of 43 (2.3 %) and 0 of 43 (0 %) of BPH control tissue. Strong marker expression was significantly increased in radical prostatectomy specimen (TOM20: 111/371 (29.9 %), DRP1: 89/373 (23.9 %), OPA1: 60/371 (16.2 %), <em>p</em> < 0.001) and in metastatic tissue (TOM20: 22/42 (52.4 %), DRP1: 14/42 (33.3 %), OPA1: 21/41 (51.2 %), <em>p</em> < 0.001). None of the markers demonstrated prognostic properties for RFS, OS, and DSS.</div></div><div><h3>Conclusion</h3><div>A strong association between the expression of the mitochondrial markers TOM20, DRP1 and OPA1 and PCa aggressiveness was demonstrated. However, these markers were not found to be prognostic regarding RFS, OS and DSS. Future studies are needed focusing on the underlying mechanisms of the upregulation of mitochondrial metabolism in aggressive PCa and evaluate potential therapeutic implications.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"13 ","pages":"Article 100131"},"PeriodicalIF":2.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142744978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study investigated the functional and translational role of long non-coding RNAs (lncRNAs), specifically MIR22HG, LNCTAM34A, and TP53TG1, in breast cancer (BC).
Methods
The expression of the lncRNAs was measured using RT-qPCR. Knockdown experiments using siRNA were conducted in breast cancer cell lines (MDA-MB-231, MDA-MB-453, and MCF-7) to assess the functional impact of silencing these lncRNAs. Cell proliferation, colony formation, invasion, migration, and apoptosis assays were performed to evaluate phenotypic changes.
Results
The expression of MIR22HG, LNCTAM34A, and TP53TG1 was significantly decreased in tumor tissues compared to NATs (p < 0.05). Lower expression of these lncRNAs correlated with advanced TNM stage and grade groups (p < 0.05). MIR22HG was overexpressed in the BC cell lines MDA-MB-231 and MCF-7, while LNCTAM34A and TP53TG1 were upregulated in MDA-MB-453 and MCF-7 BC cell lines. Silencing these lncRNAs led to a significant increase in cell proliferation, colony formation, invasion, and migration (p < 0.001). Additionally, apoptosis was significantly decreased in cells with silenced lncRNAs (p < 0.05). Knockdown of MIR22HG, LNCTAM34A, and TP53TG1 in BC cells resulted in increased cell proliferation and colony formation. Silencing of these lncRNAs significantly increased cell migration and invasion. The silencing of MIR22HG, LNCTAM34A, and TP53TG1 decreased apoptosis in BC cells.
Conclusion
Study demonstrates that MIR22HG, LNCTAM34A, and TP53TG1 function as tumor suppressors in breast cancer. Downregulation of these lncRNAs promotes tumor progression by enhancing cell proliferation, invasion, and migration, while inhibiting apoptosis.
{"title":"Silencing of long non-coding RNAs MIR22HG, LNCTAM34A, and TP53TG1 triggers cell survival/proliferation and inhibits apoptosis in women's breast cancer","authors":"Ahmed Al-Kateb , Roozbeh Heidarzadehpilehrood , Maryam Pirhoushiaran , Rasoul Abdollahzadeh , Mojtaba Saffari , Keivan Majidzadeh-A , Sepideh Mehrpoor Layeghi , Mohammad Hossein Modarressi","doi":"10.1016/j.adcanc.2025.100133","DOIUrl":"10.1016/j.adcanc.2025.100133","url":null,"abstract":"<div><h3>Background</h3><div>This study investigated the functional and translational role of long non-coding RNAs (lncRNAs), specifically MIR22HG, LNCTAM34A, and TP53TG1, in breast cancer (BC).</div></div><div><h3>Methods</h3><div>The expression of the lncRNAs was measured using RT-qPCR. Knockdown experiments using siRNA were conducted in breast cancer cell lines (MDA-MB-231, MDA-MB-453, and MCF-7) to assess the functional impact of silencing these lncRNAs. Cell proliferation, colony formation, invasion, migration, and apoptosis assays were performed to evaluate phenotypic changes.</div></div><div><h3>Results</h3><div>The expression of MIR22HG, LNCTAM34A, and TP53TG1 was significantly decreased in tumor tissues compared to NATs (<em>p</em> < 0.05). Lower expression of these lncRNAs correlated with advanced TNM stage and grade groups (<em>p</em> < 0.05). MIR22HG was overexpressed in the BC cell lines MDA-MB-231 and MCF-7, while LNCTAM34A and TP53TG1 were upregulated in MDA-MB-453 and MCF-7 BC cell lines. Silencing these lncRNAs led to a significant increase in cell proliferation, colony formation, invasion, and migration (<em>p</em> < 0.001). Additionally, apoptosis was significantly decreased in cells with silenced lncRNAs (<em>p</em> < 0.05). Knockdown of MIR22HG, LNCTAM34A, and TP53TG1 in BC cells resulted in increased cell proliferation and colony formation. Silencing of these lncRNAs significantly increased cell migration and invasion. The silencing of MIR22HG, LNCTAM34A, and TP53TG1 decreased apoptosis in BC cells.</div></div><div><h3>Conclusion</h3><div>Study demonstrates that MIR22HG, LNCTAM34A, and TP53TG1 function as tumor suppressors in breast cancer. Downregulation of these lncRNAs promotes tumor progression by enhancing cell proliferation, invasion, and migration, while inhibiting apoptosis.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"13 ","pages":"Article 100133"},"PeriodicalIF":2.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143422505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01Epub Date: 2024-10-25DOI: 10.1016/j.adcanc.2024.100129
Wei Gong , Xin Zhu , Wenwu Zhang , Xiaoyu Song , Junjie Hu , Weihua Xu , Zhichao Ma , Bin Xiao , Linhai Li , Xinping Chen
C2H2 zinc finger protein is widely involved in the occurrence and development of cancer. However, the function and mechanism of most C2H2 zinc finger proteins in breast caner (BC) remains unclear. Here, we reported the expression prognosis of C2H2 type zinc finger protein ZNF775 in BC patients and its possible biological mechanism. First, multiple public databases showed that ZNF775 was significantly overexpressed in BC tissues. Interestingly, high expression of ZNF775 was significantly associated with a better prognosis. Immunohistochemistry were used for verification, and the expression of ZNF775 was consistent with the databases. Considering the large heterogeneity of different breast cancer cells, we temporarily selected MCF-7 cell line for verification. In vitro overexpression experiments showed that overexpression of ZNF775 significantly inhibited the proliferation and migration of MCF-7 BC cell. We further combined RNA-sequencing (RNA-seq) and CUT & Tag, and found that overexpression of ZNF775 can down-regulate the expression of most genes in the Wnt signaling pathway. The cBioportal database showed that ZNF775 was negatively correlated with the expression of Wnt5a, suggesting that its downstream target was likely Wnt5a. Finally, we discovered that Wnt5a could partially reverse the inhibitory effect of ZNF775 on MCF-7 BC cell migration through transwell migration experiments. In conclusion, our findings will provide new ideas for the diagnosis, treatment and prognosis assessment of BC in the future.
C2H2 锌指蛋白广泛参与癌症的发生和发展。然而，大多数 C2H2 型锌指蛋白在乳腺癌（BC）中的功能和机制仍不清楚。在此，我们报告了C2H2型锌指蛋白ZNF775在乳腺癌患者中的表达预后及其可能的生物学机制。首先，多个公共数据库显示ZNF775在BC组织中显著过表达。有趣的是，ZNF775的高表达与较好的预后明显相关。免疫组化法进行了验证，ZNF775的表达与数据库一致。考虑到不同乳腺癌细胞的异质性较大，我们暂时选择 MCF-7 细胞系进行验证。体外过表达实验表明，过表达 ZNF775 能显著抑制 MCF-7 BC 细胞的增殖和迁移。我们进一步结合 RNA 序列分析（RNA-seq）和 CUT & Tag，发现过表达 ZNF775 可下调 Wnt 信号通路中大部分基因的表达。cBioportal数据库显示，ZNF775与Wnt5a的表达呈负相关，表明其下游靶标可能是Wnt5a。最后，我们通过经孔迁移实验发现，Wnt5a 可以部分逆转 ZNF775 对 MCF-7 BC 细胞迁移的抑制作用。总之，我们的研究结果将为今后 BC 的诊断、治疗和预后评估提供新的思路。
{"title":"ZNF775 inhibits MCF-7 breast cancer cell migration by downregulating Wnt5a","authors":"Wei Gong , Xin Zhu , Wenwu Zhang , Xiaoyu Song , Junjie Hu , Weihua Xu , Zhichao Ma , Bin Xiao , Linhai Li , Xinping Chen","doi":"10.1016/j.adcanc.2024.100129","DOIUrl":"10.1016/j.adcanc.2024.100129","url":null,"abstract":"<div><div>C2H2 zinc finger protein is widely involved in the occurrence and development of cancer. However, the function and mechanism of most C2H2 zinc finger proteins in breast caner (BC) remains unclear. Here, we reported the expression prognosis of C2H2 type zinc finger protein ZNF775 in BC patients and its possible biological mechanism. First, multiple public databases showed that ZNF775 was significantly overexpressed in BC tissues. Interestingly, high expression of ZNF775 was significantly associated with a better prognosis. Immunohistochemistry were used for verification, and the expression of ZNF775 was consistent with the databases. Considering the large heterogeneity of different breast cancer cells, we temporarily selected MCF-7 cell line for verification. In vitro overexpression experiments showed that overexpression of ZNF775 significantly inhibited the proliferation and migration of MCF-7 BC cell. We further combined RNA-sequencing (RNA-seq) and CUT & Tag, and found that overexpression of ZNF775 can down-regulate the expression of most genes in the Wnt signaling pathway. The cBioportal database showed that ZNF775 was negatively correlated with the expression of Wnt5a, suggesting that its downstream target was likely Wnt5a. Finally, we discovered that Wnt5a could partially reverse the inhibitory effect of ZNF775 on MCF-7 BC cell migration through transwell migration experiments. In conclusion, our findings will provide new ideas for the diagnosis, treatment and prognosis assessment of BC in the future.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"12 ","pages":"Article 100129"},"PeriodicalIF":2.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142571404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Colorectal cancer (CRC), currently the second most widespread cancer globally, exhibits a higher incidence in young individuals. Advancements have been made in developing anti-colorectal cancer drugs, including cytotoxic chemicals, in the past few decades. There is a need for new and innovative medications to overcome the current challenges in cancer treatment. Recent research examined the efficacy of innovative formulations in the prevention of colorectal cancer. In this study, we evaluated the efficacy of a niosome formulation loaded with Enciprazine hydrochloride (Nio-USAN). We assessed the anti-colorectal cancer characteristics of Nio-USAN by employing several techniques including CCK-8, invasion test, MTT test, flow cytometry, and cell cycle assessment. Quantitative real-time PCR was utilized to assess the transcription of genes linked to apoptosis. The F1-Nio-USAN and F2-Nio-USAN have average sizes of 200 and 500 nm, respectively. The entrapment effectiveness (EE%) of the F1-Nio-USAN and F2-Nio-USAN was measured to be 85.32 ± 0.27 % and 87.12 ± 0.35 %, respectively. The F1-Nio-USAN group exhibited the following percentages of HT-29 cell states: 43 % early apoptosis, 21 % late apoptosis, 7 % necrotic, and 29 % viable. The levels of transcription for cas8, Bid, BAX, cas9, and cas3 were significantly elevated in the treatment groups as compared to the PBS control group (P < 0.001). In addition, the treatment group exhibited significantly reduced levels of BCL2 gene transcription compared to the PBS control group (P < 0.01). These results suggest that it may be possible to improve the efficacy of USAN formulations in combating cancer by utilizing noisome encapsulation.
{"title":"Niosomes containing enciprazine hydrochloride have been shown to efficiently inhibit the proliferation and induce apoptosis in colorectal cancer cells","authors":"Hosain Nasirian , Saeedeh TarvijEslami , Hedieh Ghourchian , Marjaneh Ebrahimi , Tohid Piri-Gharaghie , Ghazal Ghajari","doi":"10.1016/j.adcanc.2024.100128","DOIUrl":"10.1016/j.adcanc.2024.100128","url":null,"abstract":"<div><p>Colorectal cancer (CRC), currently the second most widespread cancer globally, exhibits a higher incidence in young individuals. Advancements have been made in developing anti-colorectal cancer drugs, including cytotoxic chemicals, in the past few decades. There is a need for new and innovative medications to overcome the current challenges in cancer treatment. Recent research examined the efficacy of innovative formulations in the prevention of colorectal cancer. In this study, we evaluated the efficacy of a niosome formulation loaded with Enciprazine hydrochloride (Nio-USAN). We assessed the anti-colorectal cancer characteristics of Nio-USAN by employing several techniques including CCK-8, invasion test, MTT test, flow cytometry, and cell cycle assessment. Quantitative real-time PCR was utilized to assess the transcription of genes linked to apoptosis. The F1-Nio-USAN and F2-Nio-USAN have average sizes of 200 and 500 nm, respectively. The entrapment effectiveness (EE%) of the F1-Nio-USAN and F2-Nio-USAN was measured to be 85.32 ± 0.27 % and 87.12 ± 0.35 %, respectively. The F1-Nio-USAN group exhibited the following percentages of HT-29 cell states: 43 % early apoptosis, 21 % late apoptosis, 7 % necrotic, and 29 % viable. The levels of transcription for cas8, Bid, BAX, cas9, and cas3 were significantly elevated in the treatment groups as compared to the PBS control group (P < 0.001). In addition, the treatment group exhibited significantly reduced levels of BCL2 gene transcription compared to the PBS control group (P < 0.01). These results suggest that it may be possible to improve the efficacy of USAN formulations in combating cancer by utilizing noisome encapsulation.</p></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"12 ","pages":"Article 100128"},"PeriodicalIF":2.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2667394024000157/pdfft?md5=06136d00907cdb5f01bc941b96159f7d&pid=1-s2.0-S2667394024000157-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142272283","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-12-01Epub Date: 2024-10-30DOI: 10.1016/j.adcanc.2024.100130
Fatemeh Dehkhodaei , Abbas Doosti
Background
This work aims to analyze the alterations in the levels of PCA3, PCAT1, PRNCR1, and GAS5 long non-coding RNAs (lncRNAs) after the activation of pDNA-buforin II in PC3 cancer cells.
Materials and methods
The synthetic nucleic acid sequence of buforin II was included in the pcDNA3.1(+) Mammalian Expression Plasmid. The accuracy of cloning was assessed by using PCR and enzyme digestion techniques. The vectors were transfected into cells utilizing LipofectamineTM2000. The PC3 cancer cells were evaluated using flow cytometry and wound healing analysis. The expression levels of lncRNAs and apoptotic genes were assessed utilizing real-time PCR, with a significance threshold of P < 0.05.
Results
The recombinant plasmid containing the pDNA-buforin II vector was successfully generated, and the gene sequence demonstrated complete uniformity (100 % similarity) with the buforin II gene. The transfection efficiency of PC3 cells was 79 %. The results are quantified utilizing the growth inhibition 50 % (GI50) parameter, representing the concentration of pDNA-buforin II required to halt 50 % of cell growth. The percentages of early apoptosis, late apoptosis, necrosis, and viable PC3 cells in the pDNA-buforin II group were 23.30 %, 12.70 %, 3.9 %, and 60.10 %, respectively. The RT-PCR study demonstrated that the presence of pDNA-buforin II in PC3 cells decreased the transcription of PCA3, PCAT1, and PRNCR1 lncRNAs compared to the control group treated with PBS. Furthermore, it enhanced the transcription of GAS5 lncRNA. The findings demonstrated a significant upregulation of transcription factors in programmed cell death after treatment with pDNA-buforin II (∗∗P < 0.01).
Conclusions
According to the results of this study, it can be inferred that pDNA-buforin II can modify the transcription of genes in PC3 cancer cells, specifically about lncRNAs involved in cell apoptotic pathways. The pDNA-buforin II molecule has promising anticancer capabilities and can trigger apoptosis in cells.
背景本研究旨在分析 pDNA-buforin II 激活 PC3 癌细胞后 PCA3、PCAT1、PRNCR1 和 GAS5 长非编码 RNA（lncRNA）水平的变化。利用 PCR 和酶切技术评估了克隆的准确性。利用 LipofectamineTM2000 将载体转染到细胞中。使用流式细胞仪和伤口愈合分析对 PC3 癌细胞进行评估。结果pDNA-buforin II载体重组质粒成功产生，其基因序列与buforin II基因完全一致（100%相似）。PC3 细胞的转染效率为 79%。转染结果用生长抑制 50%（GI50）参数进行量化，该参数代表阻止 50% 细胞生长所需的 pDNA-buforin II 浓度。pDNA-buforin II 组早期凋亡、晚期凋亡、坏死和存活 PC3 细胞的百分比分别为 23.30%、12.70%、3.9% 和 60.10%。RT-PCR 研究表明，与用 PBS 处理的对照组相比，pDNA-buforin II 在 PC3 细胞中的存在降低了 PCA3、PCAT1 和 PRNCR1 lncRNA 的转录。此外，它还增强了 GAS5 lncRNA 的转录。结论根据本研究的结果，可以推断 pDNA-buforin II 可以改变 PC3 癌细胞中基因的转录，特别是参与细胞凋亡通路的 lncRNA。pDNA-buforin II 分子具有很好的抗癌能力，能引发细胞凋亡。
{"title":"The effect of pDNA-Buforin II on the expression changes of lncRNAs PCA3, PCAT1, PRNCR1, GAS5 in prostate cancer","authors":"Fatemeh Dehkhodaei , Abbas Doosti","doi":"10.1016/j.adcanc.2024.100130","DOIUrl":"10.1016/j.adcanc.2024.100130","url":null,"abstract":"<div><h3>Background</h3><div>This work aims to analyze the alterations in the levels of <em>PCA3</em>, <em>PCAT1</em>, <em>PRNCR1</em>, and <em>GAS5</em> long non-coding RNAs (lncRNAs) after the activation of pDNA-buforin II in PC3 cancer cells.</div></div><div><h3>Materials and methods</h3><div>The synthetic nucleic acid sequence of buforin II was included in the pcDNA3.1(+) Mammalian Expression Plasmid. The accuracy of cloning was assessed by using PCR and enzyme digestion techniques. The vectors were transfected into cells utilizing LipofectamineTM2000. The PC3 cancer cells were evaluated using flow cytometry and wound healing analysis. The expression levels of lncRNAs and apoptotic genes were assessed utilizing real-time PCR, with a significance threshold of P < 0.05.</div></div><div><h3>Results</h3><div>The recombinant plasmid containing the pDNA-buforin II vector was successfully generated, and the gene sequence demonstrated complete uniformity (100 % similarity) with the buforin II gene. The transfection efficiency of PC3 cells was 79 %. The results are quantified utilizing the growth inhibition 50 % (GI50) parameter, representing the concentration of pDNA-buforin II required to halt 50 % of cell growth. The percentages of early apoptosis, late apoptosis, necrosis, and viable PC3 cells in the pDNA-buforin II group were 23.30 %, 12.70 %, 3.9 %, and 60.10 %, respectively. The RT-PCR study demonstrated that the presence of pDNA-buforin II in PC3 cells decreased the transcription of <em>PCA3</em>, <em>PCAT1</em>, and <em>PRNCR1</em> lncRNAs compared to the control group treated with PBS. Furthermore, it enhanced the transcription of <em>GAS5</em> lncRNA. The findings demonstrated a significant upregulation of transcription factors in programmed cell death after treatment with pDNA-buforin II (∗∗P < 0.01).</div></div><div><h3>Conclusions</h3><div>According to the results of this study, it can be inferred that pDNA-buforin II can modify the transcription of genes in PC3 cancer cells, specifically about lncRNAs involved in cell apoptotic pathways. The pDNA-buforin II molecule has promising anticancer capabilities and can trigger apoptosis in cells.</div></div>","PeriodicalId":72083,"journal":{"name":"Advances in cancer biology - metastasis","volume":"12 ","pages":"Article 100130"},"PeriodicalIF":2.0,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142571405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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