Cancer Cell International最新文献

{"title":"The collagen-modifying enzyme GLT25D1 is a prognostic indicator related to immunosuppression and malignant phenotypes in hepatocellular carcinoma.","authors":"Sheng Qiu, Hongdong Han, Hongmin Zhang, Mengliu Yang, Hao Wang, Ke Li, Ling Li, Gangyi Yang","doi":"10.1186/s12935-025-03715-z","DOIUrl":"10.1186/s12935-025-03715-z","url":null,"abstract":"<p><strong>Background: </strong>The collagen β (1-O) glycosyltransferase 25 domain 1 (GLT25D1), a crucial collagen-modifying enzyme (CME), plays a pivotal role in multiple pathophysiological processes. However, its prognostic and biological roles in hepatocellular carcinoma (HCC) have not been reported.</p><p><strong>Methods: </strong>CME-related genes (CMEGs) were obtained from the Molecular Signatures Database (MSigDB), differentially expressed CMEGs (DECMEGs) and prognostic ones were identified. GLT25D1 expression was determined at the mRNA and protein levels in multiple datasets and in our HCC cohort. Its prognostic performance was evaluated and the immune microenvironment was investigated. The effects of GLT25D1 on tumorigenesis were further explored via in vitro and in vivo experiments.</p><p><strong>Results: </strong>Four potential prognosis-associated DECMEGs, including GLT25D1, were identified. GLT25D1 was noticeably up-regulated in HCC tissues and significantly associated with advanced tumor grade and stage. Enrichment analysis revealed that GLT25D1 could participate in regulating immune responses and various carcinogenic processes. HCC patients with high GLT25D1 expression had decreased CD8⁺ T cells and increased M0 macrophages, leading to an immunosuppressive microenvironment. Our in vivo and in vitro experiments confirmed the increased GLT25D1 expression, and GLT25D1 knockdown impaired the HCC malignant phenotypes.</p><p><strong>Conclusions: </strong>Our results showed that GLT25D1 could be a carcinogenic indicator reflecting poor prognosis and might serve as a potential risk biomarker for HCC patients.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"84"},"PeriodicalIF":5.3,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889767/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584662","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}

{"title":"HNRNPC promotes progression of non-small cell lung cancer by maintaining TFAP2A mRNA stability.","authors":"Minghua Liao, Chunyu Li, Rui Yang, Jun Li, Ke Wu, Jiayi Zhang, Qian Zhu, Yingchang Shi, Xianming Zhang","doi":"10.1186/s12935-025-03660-x","DOIUrl":"10.1186/s12935-025-03660-x","url":null,"abstract":"<p><strong>Background: </strong>HNRNPC is an RNA-binding protein that is overexpressed in a variety of cancers and is well known as an m6A \"reader\", but its specific function and molecular mechanism in NSCLC have not been fully understood. This study aimed to discuss molecular mechanism of HNRNPC in NSCLC.</p><p><strong>Methods: </strong>HNRNPC expression and clinically relevant data in pan-cancer and LUAD were extracted through these websites, including UALCAN, TIMER2 and GEPIA. The target gene of HNRNPC were identified through RIP-seq, meRIP-qPCR and mRNA stability test. The differential expression of target gene in NSCLC was explored by immunohistochemistry. Lentivirus was selected to knock down HNRNPC and plasmid was selected to overexpress downstream target genes. The transfection efficiency was verified by RT-qPCR and Western Blot. In vitro colony formation assay, CCK-8, wound healing, transwell assays were performed to determine the biological functions of HNRNPC and target gene in lung adenocarcinoma cells.</p><p><strong>Results: </strong>HNRNPC can promotes the expression of TFAP2A by recognizing the m6A modification of TFAP2A mRNA and maintaining its stability, activates the TFAP2A/CTNNB1 axis, enhances EMT, and ultimately promotes the malignant process of NSCLC and promote distant metastasis of NSCLC.</p><p><strong>Conclusions: </strong>These results supported that HNRNPC regulate TFAP2A to promote the malignant progression and EMT of NSCLC. These findings connect m6A modification with EMT, providing a new perspective on the regulation of m6A modification in tumors.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"85"},"PeriodicalIF":5.3,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889907/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584689","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}

{"title":"Complicated crosstalk between HMGA and non-coding RNAs modulates hallmarks of cancer.","authors":"Lijie Zhang, Xiaomin Zhao, Xianghong Gao, Hao Qin, Feng Chen, Zhijuan Lin","doi":"10.1186/s12935-025-03713-1","DOIUrl":"10.1186/s12935-025-03713-1","url":null,"abstract":"<p><p>High mobility group A1 (HMGA1) is a class of non-histone chromosomal protein and is highly expressed in the embryonic period and many tumors. It is involved in multiple hallmarks of tumors and affects the occurrence and progression of tumors. Nowadays, many non-coding RNAs (ncRNAs), such as miRNA, lncRNA, and circRNA, have been found to play a crucial role in HMGA1 regulation. Moreover, some ncRNAs are reported to be the downstream effectors of HMGA1. They interact with each other to affect multiple hallmarks of cancer and targeting ncRNAs or HMGA1 may provide potential strategies for cancer therapy. In this review, we give an overview of recent studies describing the crosstalk between oncogenic HMGA1 and ncRNAs. We also point out the impact of this interaction on the biological behavior of tumors and their potential in tumor therapy in order to offer potential implications and directions for both basic science and clinical applications.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"80"},"PeriodicalIF":5.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11887209/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584555","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}

{"title":"JAK/STAT signaling as a key regulator of ferroptosis: mechanisms and therapeutic potentials in cancer and diseases.","authors":"Yimeng Dai, Chunguo Cui, Dan Jiao, Xuewei Zhu","doi":"10.1186/s12935-025-03681-6","DOIUrl":"10.1186/s12935-025-03681-6","url":null,"abstract":"<p><p>Ferroptosis is a distinct form of regulated cell death characterized by iron-dependent lipid peroxidation, playing a critical role in various diseases, including cancer, neurodegeneration, and tissue damage. This study reviews the intricate relationship between ferroptosis and the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway, highlighting its regulatory functions across multiple biological processes. Dysregulation of the JAK/STAT pathway is implicated in promoting or inhibiting ferroptosis, depending on the context. JAK2 promotes ferroptosis by activating STAT proteins, modulating the expression of key regulators like SLC7A11 and GPX4, and influencing iron homeostasis through pathways such as ferritinophagy and hepcidin regulation. STAT1 activation primarily enhances ferroptosis through the suppression of cystine-glutamate antiporter (System Xc^-), leading to glutathione depletion and lipid peroxidation, contributing to cell death in conditions like Sjogren's syndrome and age-related macular degeneration. In contrast, STAT3 plays a protective role by upregulating SLC7A11 and GPX4, which inhibits ferroptosis and promotes cell survival, particularly in cancers such as hepatocellular carcinoma, prostate cancer, and renal cell carcinoma. This study also discusses STAT6's involvement in ferroptosis suppression in diseases like asthma and lung injury by regulating antioxidant defenses. Furthermore, the review explores potential therapeutic strategies targeting the JAK/STAT pathway to manipulate ferroptosis for disease treatment. In cancer therapy, modulating this pathway can enhance the effectiveness of ferroptosis inducers, offering promising avenues to overcome drug resistance. Additionally, the interplay between ferroptosis and JAK/STAT signaling in immune responses, oxidative stress, and lipid metabolism underscores its significance in disease progression and therapeutic intervention. By exploring these mechanisms, this study provides insights into the development of novel treatments targeting ferroptosis through JAK/STAT modulation, with implications for cancer, inflammatory diseases, and neurodegenerative conditions.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"83"},"PeriodicalIF":5.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11889932/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584661","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}

{"title":"Integrating spatial and single-cell transcriptomes reveals the role of COL1A2(+) MMP1(+/-) cancer-associated fibroblasts in ER-positive breast cancer.","authors":"Zhi-Hao Yu, Huan-Ling Xu, Shuo Wang, Ying-Xi Li, Gui-Xin Wang, Yao Tian, Zhao-Hui Chen, Wen-Bin Song, Long He, Xin Wang, Xu-Chen Cao, Yue Yu","doi":"10.1186/s12935-025-03705-1","DOIUrl":"10.1186/s12935-025-03705-1","url":null,"abstract":"<p><p>Cancer-associated fibroblasts (CAFs) are highly heterogeneous cells and important components of the breast tumor microenvironment (TME). However, their role and clinical value in ER-positive breast cancer have not been fully clarified. Our study aims to comprehensively characterize the heterogeneity, potential biological functions, and molecular mechanisms of CAFs in ER-positive breast cancer within the tumor microenvironment using multi-omics data, to provide new strategies for the diagnosis and treatment of ER-positive breast cancer patients. In this study, we found that COL1A2(+) MMP1(+) and COL1A2(+) MMP1(-) CAFs were associated with unfavorable prognosis. The dynamic evolution and cell-cell communications of CAFs were analyzed, revealing that COL1A2(+) MMP1(+/-) CAFs show extensive crosstalk with tumor-associated macrophages (TAMs), contributing to an immunosuppressive TME. Moreover, the somatic mutation of TP53 may be a potential indicator for evaluating the infiltration of COL1A2(+) MMP1(+/-) CAFs. Finally, an MRI-based radiomic model was constructed to estimate the abundance of these CAFs. In conclusion, our findings provide a theoretical basis for targeting CAFs and offer a noninvasive approach to evaluate the infiltration level of COL1A2(+) MMP1(+/-) CAFs.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"82"},"PeriodicalIF":5.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11887395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584701","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}

{"title":"Aniline TFPA enhances camptothecin-induced anti-NSCLC by modulating oxidative stress and impairing autophagy.","authors":"Han-Lin Chou, I-Ling Lin, Yei-Tsung Chen, Wen-Tsan Chang, Ann Yu, Wei-Chun Chen, Chang-Yi Wu, Shean-Jaw Chiou, Chih-Wen Shu, Chien-Chih Chiu, Pei-Feng Liu","doi":"10.1186/s12935-025-03657-6","DOIUrl":"10.1186/s12935-025-03657-6","url":null,"abstract":"<p><strong>Background: </strong>Camptothecin (CPT) derivatives are widely used in cancer therapies, but their efficacy can be attenuated by resistance mechanisms such as autophagy. We recently showed that the aniline compound 4-[4-(4-aminophenoxy)-2,3,5,6-tetrafluorophenoxy] aniline (TFPA) can potently increase CPT cytotoxicity against non-small cell lung cancer (NSCLC) cells. The purpose of this study was to evaluate whether TFPA improves CPT-based chemotherapy by modulating autophagy and other cell death pathways in NSCLC models.</p><p><strong>Methods: </strong>Two NSCLC cell lines, A549 and H1299, were tested. The synergism of CPT and TFPA was evaluated by trypan blue exclusion and colony formation assays. Annexin V staining was used for the detection of apoptosis, and autophagy was assessed by acridine orange staining and immunofluorescence. Flow cytometry-based dihydroethidium staining was used to assess oxidative stress. Changes in the expression of apoptosis-associated factors and autophagy-associated factors were determined by Western blot assays. The synergism of CPT and TFPA was validated using a zebrafish xenograft assay.</p><p><strong>Results: </strong>The accumulation of markers for lysosomal expansion (LAMP2) and degradation (cathepsin D) and markers for autophagosome formation (LC3B-II) suggested that blockage of autolysosome formation might impair autophagy in CPT-treated NSCLC cells and subsequently lead to autophagic cell death. Cotreatment with TFPA and CPT induced cell death by increasing the production of reactive oxygen species, which contributed to autophagic impairment and eventually apoptotic cell death in NSCLC cells.</p><p><strong>Conclusions: </strong>Our present work suggests that increased autophagic impairment induced by the combination of CPT and TFPA contributes to the apoptotic cell death of lung cancer cells.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"81"},"PeriodicalIF":5.3,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11887371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584597","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}

{"title":"Repurposing pitavastatin and atorvastatin to overcome chemoresistance of metastatic colorectal cancer under high glucose conditions.","authors":"Wei-Ming Cheng, Po-Chen Li, Minh Tran-Binh Nguyen, Yu-Teng Lin, Yu-Tang Huang, Tai-Shan Cheng, Thi-Huong Nguyen, Thu-Ha Tran, Tzu-Yi Huang, Thu-Huyen Hoang, Sin-Yu Chen, Yu-Chieh Chu, Chih-Wei Wu, Ming-Fen Lee, Yi-Shiou Chiou, Hsiao-Sheng Liu, Yi-Ren Hong, Peter Mu-Hsin Chang, Yu-Feng Hu, Ying-Chih Chang, Jin-Mei Lai, Chi-Ying F Huang","doi":"10.1186/s12935-025-03712-2","DOIUrl":"10.1186/s12935-025-03712-2","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) poses a significant clinical challenge because of drug resistance, which can adversely impact patient outcomes. Recent research has shown that abnormalities within the tumor microenvironment, especially hyperglycemia, play a crucial role in promoting metastasis and chemoresistance, and thereby determine the overall prognosis of patients with advanced CRC.</p><p><strong>Methods: </strong>This study employs data mining and consensus molecular subtype (CMS) techniques to identify pitavastatin and atorvastatin as potential agents for targeting high glucose-induced drug resistance in advanced CRC cells. CRC cells maintained under either low or high glucose conditions were established and utilized to assess the cytotoxic effects of pitavastatin and atorvastatin, both with and without 5-fluorouracil (5-FU). CRC 3D spheroids cultured were also included to demonstrate the anti-drug resistance of pitavastatin and atorvastatin.</p><p><strong>Results: </strong>A bioinformatics analysis identified pitavastatin and atorvastatin as promising drug candidates. The CMS4 CRC cell line SW480 (SW480-HG) was established and cultured under high glucose conditions to simulate hyperglycemia-induced drug resistance and metastasis in CRC patients. Pitavastatin and atorvastatin could inhibit cell proliferation and 3D spheroid formation of CMS4 CRC cells under high glucose conditions. In addition, both pitavastatin and atorvastatin can synergistically promote the 5-FU-mediated cytotoxic effect and inhibit the growth of 5-FU-resistant CRC cells. Mechanistically, pitavastatin and atorvastatin can induce apoptosis and synergistically promote the 5-FU-mediated cytotoxic effect by activating autophagy, as well as the PERK/ATF4/CHOP signaling pathway while decreasing YAP expression.</p><p><strong>Conclusion: </strong>This study highlights the biomarker-guided precision medicine strategy for drug repurposing. Pitavastatin and atorvastatin could be used to assist in the treatment of advanced CRC, particularly with CMS4 subtype CRC patients who also suffer from hyperglycemia. Pitavastatin, with an achievable dosage used for clinical interventions, is highly recommended for a novel CRC therapeutic strategy.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"79"},"PeriodicalIF":5.3,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11887183/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572158","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}

{"title":"Triple-positive breast cancer: navigating heterogeneity and advancing multimodal therapies for improving patient outcomes.","authors":"Jie Xie, Zhihui Yang, Zhuolin Li, Tianyu Zhang, Huan Chen, Xueru Chen, Zehua Dai, Tao Chen, Jing Hou","doi":"10.1186/s12935-025-03680-7","DOIUrl":"10.1186/s12935-025-03680-7","url":null,"abstract":"<p><p>Triple-positive breast cancer (TPBC), a unique subtype of luminal breast cancer, is characterized by concurrent positivity for estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). Owing to the crosstalk between the ER and HER2 signaling pathways, the standard of care and drug resistance of this particular subtype are difficult challenges. Recent research and clinical trials have indicated a shift in the treatment paradigm for TPBC from single-target therapies to multi-pathway, multitarget strategies aiming to comprehensively modulate intricate signaling networks, thereby overcoming resistance and enhancing therapeutic outcomes. Among multiple strategies, triple-drug therapy has emerged as a promising treatment modality, demonstrating potential efficacy in patients with TPBC. Moving forward, there is a critical need to perform in-depth analyses of specific mechanisms of cancer pathogenesis and metastasis, decipher the complex interactions between different genes or proteins, and identify concrete molecular targets, thus paving the way for the development of tailored therapeutic strategies to combat TPBC effectively.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"77"},"PeriodicalIF":5.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143566216","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}

{"title":"The emerging role of glycolysis and immune evasion in ovarian cancer.","authors":"Bowen Jin, Zehua Miao, Junjie Pan, Zhen Zhang, Yibei Yang, Yidong Zhou, Yuanxiang Jin, Zheng Niu, Qiaoping Xu","doi":"10.1186/s12935-025-03698-x","DOIUrl":"10.1186/s12935-025-03698-x","url":null,"abstract":"<p><p>Ovarian cancer (OC) is one of the three most common malignant tumors of the female reproductive system, with the highest mortality rate among gynecologic malignancies. Like other tumors, OC cells undergo metabolic reprogramming phenomenon and convert glucose metabolism into \"aerobic glycolysis\" and generate a high concentration of lactate, i.e., the \"Warburg effect\", which provides a large amount of energy and corresponding intermediary metabolites for their survival, reproduction and metastasis. Numerous studies have shown that targeted inhibition of aerobic glycolysis and lactate metabolism is a promising strategy to enhance the sensitivity of cancer cells to immunotherapy. Therefore, this review summarizes the metabolic features of glycolysis in OC cells and highlights how abnormal lactate concentration affects the differentiation, metabolism, and function of infiltrating immune cells, which contributes to immunosuppression, and how targeted inhibition of this phenomenon may be a potential strategy to enhance the therapeutic efficacy of OC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"78"},"PeriodicalIF":5.3,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11881340/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143566211","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}

{"title":"Unveiling the oncogenic role of SLC25A13: a multi-omics pan-cancer analysis reveals its impact on glioma progression.","authors":"Wenjie Wu, Simin Liu, Huili Ren, Yuxin Rao, Jun Nie, Keke Wei, Xiaobing Jiang","doi":"10.1186/s12935-025-03696-z","DOIUrl":"10.1186/s12935-025-03696-z","url":null,"abstract":"<p><p>SLC25A13, a pivotal component of the mitochondrial aspartate-glutamate carrier, is integral to cellular metabolism and has been linked to various diseases. However, its role in cancer biology remains largely unexplored. In this study, we employed multi-omics data to elucidate the genetic landscape, expression profile, and prognostic value of SLC25A13 in a pan-cancer context. Additionally, we examined the correlation between SLC25A13 and the immune microenvironment across various cancers. By applying multiple machine learning methods, we identified seven core SLC25A13 co-expressed genes and developed a nomogram to predict the prognosis of glioma patients, validating its efficacy across multiple independent datasets. Furthermore, in vitro and in vivo experiments demonstrated that SLC25A13 is significantly overexpressed in glioblastoma tissues compared to paraneoplastic tissues, promoting glioblastoma cell proliferation and migration while inhibiting apoptosis. Collectively, our study positions SLC25A13 as a promising biomarker for cancer prognosis and a potential therapeutic target, particularly in glioma, thereby laying the groundwork for future research into its therapeutic exploitation in cancer.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"76"},"PeriodicalIF":5.3,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11874833/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540374","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}