Cancer Biology & Therapy最新文献

{"title":"Suppression of pseudogene MT2P1 transcription induced by E2F7 inhibits hepatocellular carcinoma cell proliferation and facilitates apoptosis via preserving its parental gene.","authors":"Yiquan Lu, Yifan Zhang, Fengjie Hao, Nan Wang, Yongjun Chen, Junqing Wang","doi":"10.1080/15384047.2025.2510035","DOIUrl":"10.1080/15384047.2025.2510035","url":null,"abstract":"<p><p>The majority of the pseudogenes are inert in normal transcription. Their transcripts are mostly attributed to non-coding RNAs that play various functions in human tumorigenicity and progression. Distinctively, pseudogene MT2P1 is universally transcribed in hepatocytes and presents a significant decrease in hepatocellular carcinoma (HCC). The effect of MT2P1-RNA on HCC cell proliferation and apoptosis needs investigation. MT2P1-RNA was detected by RT-qPCR assay in HCC tissues and cell lines, combined with the exploration of the public databases. The immunohistochemistry assay was used for testing the expression profile of E2F7 and the parental gene MT2A. The clinicopathological features of the patients were collected and analyzed. Ectopic expression of MT2P1-RNA in HCC cell lines was conducted, and the CCK8 assay and flow cytometry assay were carried out. Chromatin immunoprecipitation assay and Dual-luciferase reporter assay were, respectively, applied to validate the interaction between MT2P1, E2F7, and microRNA-15b-5p. The downregulation of MT2P1-RNA in HCC is negatively correlated with dismal clinicopathological features. MT2P1-RNA significantly suppressed HCC cell proliferation and induced apoptosis. E2F7 depletion sequentially elevated the level of MT2P1-RNA and MT2A, and E2F7 was validated as a suppressive transcription factor of the MT2P1 gene. The direct interactions of either MT2P1/miR-15b-5p or miR-15b-5p/MT2A were, respectively, ascertained, enlightening the ceRNA effect of them. The pseudogene-derived MT2P1-RNA is a suppressor of HCC by exerting the ceRNA effect on preserving MT2A, and its transcription is regulated by the suppressive transcription factor E2F7.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2510035"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12118385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144126816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Copper death combination therapy: the innovative frontier and challenges in prostate cancer treatment.","authors":"Jia Wei He, Pei Zhen Li, Zi Xuan Huang","doi":"10.1080/15384047.2025.2532224","DOIUrl":"10.1080/15384047.2025.2532224","url":null,"abstract":"<p><p>Prostate cancer (PCA) remains a significant health challenge, necessitating the exploration of novel therapeutic strategies to enhance patient outcomes. Recent research has identified cuproptosis, a copper-dependent programmed cell death mechanism, as a promising target in PCA treatment. Elevated copper levels have been associated with tumor progression and therapeutic resistance, highlighting the need for innovative approaches. This review synthesizes current findings on the role of copper and cuproptosis in PCA, focusing on the mechanisms underlying cuproptosis, the identification of key biomarkers, and the therapeutic potential of copper complexes and ionophores. The integration of cuproptosis-related biomarkers into clinical practice may facilitate personalized treatment strategies, while ongoing research into copper-based therapies holds promise for overcoming limitations of traditional chemotherapy. Future directions should emphasize elucidating the molecular mechanisms of cuproptosis and optimizing therapeutic applications to improve patient outcomes in PCA.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2532224"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269702/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144636226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Robust prediction of glioma prognosis by hypoxia-induced ferroptosis genes: VEGFA-XBP1 co-expression for salvage therapy.","authors":"Zhou Liwei, Lu Hanwen, Zhao Wenpeng, Yu Weijie, Chen Sifang, Zhang Bingchang, Li Zhangyu, Gao Xin, Li Wenhua, Mao Jianyao, Xie Yuanyuan, Tan Guowei, Wang Zhanxiang","doi":"10.1080/15384047.2025.2529643","DOIUrl":"10.1080/15384047.2025.2529643","url":null,"abstract":"<p><p>Hypoxia as a hallmark of solid malignancies compromises therapeutic efficacy and prognosis. This study deciphers the functional role of hypoxia-induced ferroptosis in glioma prognosis. Hypoxia-related transcripts and ferroptosis markers were curated from public databases. ConsensusClusterPlus identify hypoxia-based molecular subtypes, while LASSO-penalized Cox regression integrated with limma-based differential expression analysis screened prognostic ferroptosis genes. Subsequent risk modeling was validated against clinical parameters and extended through nomogram construction. Protein-protein interaction networks centered on HIF-1αidentified high-confidence interactors, with parallel immune correlation analysis completing the systems-level investigation.Based on 27 hypoxia-associated genes, we stratified samples into three distinct hypoxic clusters. Differential analysis of 123 ferroptosis markers across clusters, combined with univariate Cox regression and LASSO regression, identified 23 hypoxia-induced ferroptosis genes for constructing a prognostic model. The model demonstrated robust predictive accuracy with AUC values of 0.80 (1-year), 0.86 (3-year), and 0.86 (5-year). GSEA revealed significant enrichment in ECM-receptor interactions, focal adhesion, JAK-STAT signaling, and p53 signaling pathways, suggesting their involvement in hypoxia-induced ferroptosis. Our risk model significantly outperformed conventional clinical parameters (pathology, grade, age, primary/recurrent status). Protein-protein interaction analysis incorporating HIF-1αand the 23-model genes identified XBP1 and VEGFA co-expression as significant positive prognostic factor. The immune infiltration analysis further indicated that M0 macrophages may participate in the regulation of the prognosis of VEGFA-XBP1.Hypoxia-induced ferroptosis modulation emerges as a prognostic factor in gliomas, with XBP1 and VEGFA representing druggable nodes for novel combination therapies.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2529643"},"PeriodicalIF":4.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12239816/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144574882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NR4A3 regulates anoikis resistance and metastasis of bladder cancer through EWSR1.","authors":"Li Fan, Yulin Zhou, Shouyong Liu, Xinfeng Zhuo, Le Qu, Ding Wu, Suchun Wang, Xin Pan, Tangliang Zhao, Feng Xu, Jingping Ge, Wenquan Zhou","doi":"10.1080/15384047.2025.2535774","DOIUrl":"10.1080/15384047.2025.2535774","url":null,"abstract":"<p><p>Bladder cancer (BLCA) is a common urinary malignancy with high metastatic potential. However, the mechanisms underlying its progression remain unclear. This study aimed to investigate the role and regulatory mechanisms of NR4A3, a nuclear receptor involved in apoptosis and tumor suppression, in BLCA progression, particularly its impact on anoikis resistance and metastasis. NR4A3 expression levels were analyzed using the GEPIA database. Functional studies were conducted by overexpressing NR4A3 in adherent and suspension-cultured BLCA cells. Apoptosis, invasion, migration, and ER stress marker (Bip and CHOP) expression were evaluated. Subcutaneous and lung metastasis models in BALB/c nude mice were used for in vivo validation. GEPIA analysis showed that NR4A3 is significantly downregulated in BLCA. NR4A3 overexpression increased apoptosis, reduced invasion and migration, and upregulated Bip and CHOP expression. <i>In vivo</i>, NR4A3 overexpression significantly reduced lung metastasis in BALB/c nude mice (<i>n</i> = 8 per group, <i>p</i> < .001). Mechanistically, NR4A3 promoted ER stress by regulating the EWSR1/Ezrin pathway, thereby suppressing anoikis resistance. NR4A3 functions as a tumor suppressor in BLCA by enhancing endoplasmic reticulum stress and inhibiting anoikis resistance through the EWSR1/Ezrin pathway. It may serve as a promising therapeutic target for metastatic BLCA.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2535774"},"PeriodicalIF":4.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12326571/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-135a-3p inhibits the progression of prostate cancer by targeting TLR4.","authors":"LianQiang Li, Xiao Zhang","doi":"10.1080/15384047.2025.2545653","DOIUrl":"https://doi.org/10.1080/15384047.2025.2545653","url":null,"abstract":"<p><p>To explore the expression of miR-135a-3p in prostate cancer，analyze its effects on tumor development and the involved mechanisms. A total of 125 specimens of cancer tissues and corresponding adjacent normal tissues from prostate cancer patients were collected. Real - Time quantitative PCR was employed to quantify the expression levels of miR-135a-3p in prostate cancer tissues and cell lines. Kaplan-Meier survival curve analysis and Cox regression were performed to evaluate the prognostic significance of miR-135a-3p in prostate cancer. The CCK-8 assay was used to detect cell proliferation. A dual-luciferase reporter assay was employed to validate the targeting interaction between miR-135a-3p and Toll-like receptor 4 (TLR4). miR-135a-3p is lowly expressed in prostate cancer tissues and cells, and its low expression is associated with poor prognosis of patients. The low expression state of miR-135a-3p showed a significant correlation with TNM stage, clinical stage, Gleason score, and lymph node metastasis. In addition, miR-135a-3p inhibits the proliferation of prostate cancer cells and cancer progression by negatively regulating the expression of TLR4. miR-135a-3p is downregulated in prostate cancer and is associated with poor prognosis of patients. It exerts an inhibitory effect on the progression of prostate cancer by targeting TLR4.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2545653"},"PeriodicalIF":4.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12377118/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144943467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sulfatase 2 inhibition sensitizes triple-negative breast cancer cells to paclitaxel through augmentation of extracellular ATP.","authors":"Jasmine M Manouchehri, Jharna Datta, Lynn M Marcho, Daniel Stover, Ramesh K Ganju, Bhuvaneswari Ramaswamy, William E Carson, Arjun Mittra, Xiaoli Zhang, Patrick M Schnell, Yu Yue, Mark P Rubinstein, Mathew A Cherian","doi":"10.1080/15384047.2025.2483989","DOIUrl":"10.1080/15384047.2025.2483989","url":null,"abstract":"<p><p>The highest incidence and cancer-related mortality rate among women worldwide is due to breast cancer. Triple-negative breast cancers (TNBC) are associated with more inferior outcomes than other breast cancers because of their progressive nature and the deficit in available therapies. Therefore, there is a need for new therapeutic approaches. Our lab determined that chemotherapy induces the release of extracellular adenosine triphosphate (eATP), and, hence, augments TNBC cells' response to chemotherapy. Despite this, eATP concentrations are restricted by a variety of extracellular ATPases. We propose that, as an ATPase inhibitor, heparan sulfate (HS) would augment eATP concentrations and TNBC vulnerability induced by chemotherapy. Sulfatase 2 (SULF2) removes sulfate from HS, the functional group essential for ATPase inhibition. Consequently, we propose that TNBC cell death and eATP release induced by chemotherapy would be intensified by SULF2 inhibitors. We examined eATP and cell viability in paclitaxel-treated TNBC and nontumorigenic immortal mammary epithelial MCF-10A cells in the presence of OKN-007, a selective SULF2 inhibitor, and/or heparan sodium sulfate. Furthermore, sulfatase 1 (SULF1) and SULF2 protein expressions were ascertained. We found that the expression of SULF2 was greater in TNBC cell lines when compared to MCF-10A cells. The release of eATP and loss of TNBC cell viability induced by chemotherapy was enhanced by OKN-007. The co-treatment of chemotherapy and OKN-007 also attenuated cancer-initiating cells. This data implies that the combination of SULF2 inhibitors with chemotherapy augments eATP and decreases cell viability of TNBC greater than chemotherapy alone.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2483989"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11951697/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143718171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancements in exosome-based cancer diagnosis: from chipsets to nano vaccine.","authors":"Nobendu Mukerjee, Subham Sarkar, Daniel Ejim Uti, Prashant Kumar Sharma","doi":"10.1080/15384047.2025.2541991","DOIUrl":"10.1080/15384047.2025.2541991","url":null,"abstract":"<p><p>Exosome-based therapies represent a pioneering frontier in cancer treatment, leveraging the natural cellular communication mechanisms encapsulated in exosomes. These nano-sized vesicles serve as carriers of proteins, lipids, and nucleic acids, reflecting the physiological state of their cells of origin, which makes them ideal candidates for targeted cancer therapies and diagnostics. Despite their potential, the path to clinical application is fraught with challenges. This review explores the inherent challenges associated with exosome-based cancer vaccines, focusing on tumor heterogeneity, the technical difficulties in exosome isolation and characterization, the need for standardized protocols, and the scalability of production methods. It also explores the interaction between exosomes and the immune system, a crucial factor in developing effective cancer vaccines. The review explores strategies to improve diagnostic tools, targeted delivery systems, and therapy based on individual tumor profiles, highlighting the need for innovative approaches and collaborative efforts to maximize exosome-based cancer vaccines' therapeutic potential.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2541991"},"PeriodicalIF":4.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12323433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NVP-2, in combination with Orlistat, represents a promising therapeutic strategy for acute myeloid leukemia.","authors":"Qing Zhu, Jia Cheng, Yuqing Gao, Zimu Zhang, Jian Pan, Xin Su, Danhong Fei, Linbo Cai, Juanjuan Yu, Yanling Chen, Wanyan Jiao, Di Wu, Xiaolu Li, Peifang Xiao","doi":"10.1080/15384047.2025.2450859","DOIUrl":"10.1080/15384047.2025.2450859","url":null,"abstract":"<p><p>Cell cycle dysregulation and the corresponding metabolic reprogramming play significant roles in tumor development and progression. CDK9, a kinase that regulates gene transcription and cell cycle, also induces oncogene transcription and abnormal cell cycle in AML cells. The function of CDK9 for gene regulation in AML cells requires further exploration. In this study, we knocked down the CDK9 to investigate its effects on the growth and survival of AML cells. Through RNA-seq analysis, we identified that in U937 cells CDK9 regulates numerous genes involved in proliferation and apoptosis, including mTOR, SREBF1, and Bcl-2. Furthermore, our results demonstrated that both CDK9 and FASN are crucial for the proliferation and survival of Kasumi-1 and U937 cells. Mechanistically, MCL1, c-Myc, and Akt/mTOR/SREBF1 may be critical factors and pathways in the combined therapy of NVP-2 and Orlistat. In summary, our study revealed that CDK9 and FASN are vital for maintaining AML cell survival and proliferation. Treatment with NVP-2 and Orlistat may be a promising clinical candidate for patients with AML.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2450859"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730633/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142969552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"USP7 overexpression prevents the progression of clear cell renal cell carcinoma by enhancing pyroptosis via TRIP12 deubiquitination.","authors":"Hongsheng Li, Yao Ning, Junjie Yu, Yiju Chen, Qiang He, Juan Jin","doi":"10.1080/15384047.2025.2558402","DOIUrl":"10.1080/15384047.2025.2558402","url":null,"abstract":"<p><p>Ubiquitin-specific protease 7 (USP7) involves in various human cancers due to its capacity for binding and stabilizing specific target proteins through deubiquitylation, but its roles in clear cell renal cell carcinoma (ccRCC) development remains unknown. This study aimed to determine the role of USP7 in the pyroptosis mechanism in ccRCC, thereby providing novel anti-ccRCC strategies. Bioinformatics analysis was conducted to explore the expression of USP7 and TRIP12 in ccRCC patients and their association with patient overall survival. qRT-PCR, western blotting, and ELISA were used to determine the levels of USP7, TRIP12, pyroptosis-related factors. Cell viability, invasion, pyroptosis, and proliferation were evaluated using CCK-8, Transwell, flow cytometry, and immunohistochemistry assays. The direct interaction between USP7 and TRIP12 was validated by co-immunoprecipitation (CO-IP). We found downregulated USP7 in ccRCC tissues, which was related to the shorter patient overall survival (OS). Significantly, USP7 was also decreased in ccRCC cells. oe-USP7 (USP7 overexpression) inhibited ccRCC cell viability, migration, invasion, and enhanced pyroptosis. The caspase-1 specific inhibitor, VX-765, partially abolished the anti-viability, and pro-pyroptosis effects of oe-USP7, indicating USP7 overexpression prevented the malignant phenotype of ccRCC cells by enhancing caspase-1 dependent pyroptosis. Similarly, the shorter patient OS was indicated to be associated with reduced TRIP12 in ccRCC tissues. Besides, oe-USP7 increased TRIP12 expression in ccRCC cells by deubiquitinating TRIP12, while sh-TRIP12 eliminated the biological functions of oe-USP7. The similar effects of oe-USP7 on ccRCC development were found in ccRCC mice. USP7 mediated TRIP12 deubiquitination inhibited ccRCC progression by enhancing pyroptosis.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2558402"},"PeriodicalIF":4.6,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12439559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145063513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A pan-cancer analysis of MARCH8: molecular characteristics, clinical relevance, and immuno-oncology features.","authors":"Zihan Quan, Songqing Fan, Hongmei Zheng, Yue Ning, Yang Yang","doi":"10.1080/15384047.2025.2458773","DOIUrl":"10.1080/15384047.2025.2458773","url":null,"abstract":"<p><p>Membrane-associated RING-CH8 (MARCH8) is a member of the recently discovered MARCH family of ubiquitin ligases. MARCH8 has been shown to participate in immune responses. However, the role of MARCH8 in prognosis and immunology in human cancers remains largely unknown. The expression of MARCH8 protein was detected via immunohistochemistry in non-small cell lung cancer (NSCLC) and non-cancerous lung tissues. The study investigated the role of MARCH8 in tumor immunity through pan-cancer analysis of multiple databases. MARCH8 genetic alternations and expression were explored with the cBioPortal, GTEx, and TCGA databases. We investigated the role of MARCH8 expression in clinical relevance, prognosis, tumor immune microenvironment, immune checkpoint (ICP) with a series of bioinformatics tools and methods, such as TISIDB database, ESTIMATE, and CIBERSORT method. MARCH8 expression showed cancer-specific dysregulation and was associated with the prognosis of patients in various cancers. MARCH8 was related to the tumor microenvironment and participated in tumor immune regulation. Furthermore, low expression of MARCH8 was associated with poor prognosis and might serve as an independent prognostic biomarker for NSCLC patients. The comprehensive pan-cancer analysis revealed the potential of MARCH8 in tumor-targeted therapy, and suggested MARCH8 as a promising prognostic and immunological pan-cancer biomarker.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"26 1","pages":"2458773"},"PeriodicalIF":4.4,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11784653/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143064025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}