Cancer Cell International最新文献

{"title":"Cell-cycle-related transcriptional factor DLX4: a novel prognostic biomarker and potential therapeutic target in colorectal cancer.","authors":"Jingsong Cheng, Chengxi Zhang, Yiman Luo, Yihan Chen, Nanting Chen, Yuanyuan Wan, Xinyu Huang, Ziheng Zheng, Qingyao Yin, Xue Chen, Jing Hua, Yang Li, Rongzhong Huang","doi":"10.1186/s12935-025-03998-2","DOIUrl":"https://doi.org/10.1186/s12935-025-03998-2","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"370"},"PeriodicalIF":6.0,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145343542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The potential role of cannabidiol (CBD) in lung cancer therapy: a systematic review of preclinical and clinical evidence.","authors":"Mojtaba Esmaeli, Maryam Dehghanpour Dehabadi","doi":"10.1186/s12935-025-04010-7","DOIUrl":"https://doi.org/10.1186/s12935-025-04010-7","url":null,"abstract":"<p><strong>Background: </strong>Lung cancer is one of the most prevalent and lethal cancers worldwide, with limited therapeutic options in advanced stages. Cannabinoids have recently attracted attention as potential anticancer agents; however, cannabidiol (CBD), a non-psychoactive compound derived from Cannabis sativa, has emerged as the most promising candidate. Unlike Δ9-tetrahydrocannabinol (THC), CBD lacks psychoactive properties, is generally well tolerated, and demonstrates a favorable safety profile. Moreover, CBD influences multiple cancer-relevant pathways-including apoptosis, epithelial-to-mesenchymal transition (EMT), and immune modulation-that are particularly relevant to non-small cell lung cancer (NSCLC). These features provide a strong rationale for focusing on CBD in lung cancer therapy.</p><p><strong>Methods: </strong>A systematic search was conducted in PubMed, Scopus, Web of Science, and Google Scholar, using defined keywords such as \"CBD,\" \"lung cancer,\" and \"non-small cell lung cancer.\" Studies from 2007 to 2025 were screened following PRISMA guidelines, and 19 studies met the inclusion criteria.</p><p><strong>Results: </strong>Nineteen studies met the inclusion criteria, comprising 13 in vitro studies, 4 in vivo animal studies, and 2 clinical reports. Across these studies, CBD was administered at concentrations ranging from low micromolar levels (1-10 µM) in cell-based experiments to oral doses of 200-600 mg/day in human cases. Mechanistically, CBD induced apoptosis through pathways such as PPAR-γ activation, mitochondrial dysfunction, and oxidative stress. It inhibited epithelial-to-mesenchymal transition (EMT), downregulated invasive markers, and modulated the tumor microenvironment by enhancing CD8 + T cell and NK cell activity. Furthermore, CBD showed synergistic effects with conventional therapies (e.g., cisplatin, radiotherapy) by increasing drug uptake and overcoming resistance.</p><p><strong>Conclusions: </strong>CBD holds promise as an adjunct in lung cancer therapy, addressing key cancer hallmarks such as tumor growth, metastasis, and treatment resistance. While preclinical evidence is robust, clinical trials remain limited. Future research should focus on optimizing dosing regimens, evaluating long-term safety, and validating these findings in large-scale human studies.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"369"},"PeriodicalIF":6.0,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145343617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive phosphoproteomic profiling reveals sex-specific regulatory mechanisms in HrasG12V-driven hepatocarcinogenesis.","authors":"Changcheng Yang, Juefu Hu, Liang Yao, Yang Yu, Xiaoying Dong, Jun Chen, Aiguo Wang, Huiling Li","doi":"10.1186/s12935-025-04015-2","DOIUrl":"https://doi.org/10.1186/s12935-025-04015-2","url":null,"abstract":"<p><strong>Objective: </strong>To identify common and sex-specific phosphorylation dynamics during hepatocarcinogenesis in HrasG12V transgenic mice (Hras-Tg).</p><p><strong>Methods: </strong>We constructed a phosphoproteomic database using male/female (M/F) tumor (T), precancerous (P), and wild-type liver tissues (W) from Hras-Tg, validated via parallel reaction monitoring (PRM). Comparative analysis and hierarchical clustering were employed to delineate shared and sex-stratified phosphorylation signatures in hepatocellular carcinoma (HCC) development.</p><p><strong>Results: </strong>PRM-validated phosphoproteomic profiling quantified 5,410 phosphorylation sites across 2,427 proteins. Analysis of common features revealed nuclear-enriched phosphoprotein accumulation in tumors versus precancerous/wild-type tissues (T vs. P/W). KEGG pathway analysis identified consistently dysregulated pathways including MAPK signaling, focal adhesion, and protein digestion/absorption. Protein-protein interaction (PPI) network analysis of shared phosphoproteins pinpointed key regulators (Alb, Hspa5, Psn), with high connectivity, suggesting potential regulatory roles in the network. Sex-specific analyses demonstrated distinct phosphorylation patterns: males exhibited extensive membrane protein phosphorylation alterations, while females showed predominant cytoplasmic modifications. KEGG pathway mapping revealed male-biased dysregulation in Ras signaling, mTOR pathways, and actin cytoskeleton regulation. Functional annotation indicated greater complexity of phosphorylated proteins in males. Notably, phosphorylation events occurring on proteins with annotated kinase or phosphatase activity were more prevalent in males, suggesting enhanced phosphorylation-mediated signaling dynamics.</p><p><strong>Significance: </strong>This study establishes the first sexual dimorphism-aware phosphoproteomic resource for Ras-driven hepatocarcinogenesis, systematically characterizing conserved and sex-divergent phosphorylation networks. The findings provide preliminary molecular insights into gender disparities in HCC progression and may guide future therapeutic exploration.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"367"},"PeriodicalIF":6.0,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145343505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical pathological significance and biological functions of APIP in hepatocellular carcinoma.","authors":"Cong Yu, Jiang-Hua Huang, Rui Zhang, Kang-Lai Wei, Zhen-Bo Feng","doi":"10.1186/s12935-025-04018-z","DOIUrl":"https://doi.org/10.1186/s12935-025-04018-z","url":null,"abstract":"<p><strong>Background & aims: </strong>Hepatocellular carcinoma (HCC) is among the most common malignant tumors globally, characterized by high morbidity and mortality. This study aims to investigate the clinical and pathological significance of Apaf-1-interacting protein (APIP) expression in HCC, assess its biological effects on HCC cells, and explore the underlying mechanisms.</p><p><strong>Methods: </strong>Internal tissue samples were analyzed to determine APIP expression and its clinical relevance in HCC using real-time quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry (IHC). External datasets were employed for verification. Experiments investigating cell proliferation, cell cycle progression, apoptosis, migration, and invasion were performed to understand the biological role and molecular mechanisms of APIP in HCC cells. Additionally, upstream transcription factors regulating APIP expression were explored.</p><p><strong>Results: </strong>APIP expressionwas significantly higher in HCC tissues compared to adjacent non-tumor tissues, effectively distinguishing HCC from normal liver tissues. APIP expression correlated with age, gender, and poor prognosis in patients with HCC. Furthermore, downregulation of APIP promoted apoptosis and inhibited proliferation, migration, and invasion of HCC cells. A regulatory relationship between APIP and the transcription factor Serum Response Factor (SRF) was also identified.</p><p><strong>Conclusion: </strong>APIP significantly contributes to the initiation and progression of HCC by mediating cell proliferation, apoptosis, migration, and invasion. Therefore, APIP may serve as a potential diagnostic and prognostic biomarker for HCC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"368"},"PeriodicalIF":6.0,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145343510","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systemic chemotherapy in metastatic TNBC polarizes effector T cell differentiation.","authors":"Hye-Yeon Ju, Hyundong Yoon, Seungpil Jung, Serk In Park, Tae Kon Kim, Mi-Ryung Han","doi":"10.1186/s12935-025-04011-6","DOIUrl":"https://doi.org/10.1186/s12935-025-04011-6","url":null,"abstract":"<p><strong>Background: </strong>Triple-negative breast cancer (TNBC) has the poorest prognosis among the three major subtypes of breast cancer, and more than one-third of patients with TNBC experience recurrence or distant metastasis. Despite advances in diverse immunotherapy strategies for metastatic TNBC (mTNBC), multiple mechanisms underlying resistance to treatment remain unknown.</p><p><strong>Methods: </strong>In this study, the dynamic changes in the immune landscape in mTNBC were assessed and compared with healthy donors using single-cell RNA sequencing (scRNA-seq) analysis. By integrating internal and public scRNA-seq data, 61,149 cells extracted from East Asian patients with mTNBC and 51,448 cells extracted from East Asian healthy donors were used to landscape a comprehensive cellular profile of mTNBC.</p><p><strong>Results: </strong>Results showed that nine overexpressed genes from patients with mTNBC in effector T cells such as CTSW, PRF1, GNLY, GZMA, CCL5, KLRD1, KLRB1, B2M, and GZMB exhibited favorable survival prognoses. In addition, effector T cells enriched in patients with mTNBC were more differentiated compared with those enriched in healthy donors.</p><p><strong>Conclusion: </strong>Collectively, this study is the first to provide potential diagnostic and therapeutic targets of East Asian chemotherapy-treated mTNBC with regard to effector T cells.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"371"},"PeriodicalIF":6.0,"publicationDate":"2025-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145343616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metal ion transporter SLC39A14-mediated ferroptosis and glycosylation modulate the tumor immune microenvironment: pan-cancer multi-omics exploration of therapeutic potential.","authors":"Yi-Chun Chiang, Chih-Yang Wang, Sachin Kumar, Chung-Bao Hsieh, Kai-Fu Chang, Ching-Chung Ko, Chih-Hsuan Chang, Hui-Ru Lin, Chi-Jen Wu, Chien-Han Yuan, Do Thi Minh Xuan, Juan Lorell Ngadio, Dahlak Daniel Solomon, Fitria Sari Wulandari, Hung-Yun Lin, Shun-Fa Yang, Yung-Kuo Lee","doi":"10.1186/s12935-025-04003-6","DOIUrl":"https://doi.org/10.1186/s12935-025-04003-6","url":null,"abstract":"<p><strong>Background: </strong>Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has emerged as a pivotal mechanism in cancer progression and therapeutic resistance. Concurrently, glycosylation, as a key post-translational modification, plays a critical role in regulating cell signaling, immune evasion, and metastasis. Although both processes are independently implicated in tumor biology, the intersection between ferroptosis and glycosylation remains largely unexplored.</p><p><strong>Methods: </strong>We performed a comprehensive pan-cancer multi-omics analysis, integrating bulk transcriptomics, epigenomics, and single-cell RNA sequencing datasets. Ferroptosis and glycosylation-related genes were curated from The Molecular Signatures Database (MSigDB), leading to the identification of the metal ion transporter, SLC39A14 (solute carrier family 39 member 14), as a key intersecting gene. A ferroptosis-related gene signature was constructed using machine learning and Cox regression models, followed by survival analyses, immune microenvironment profiling, and a pathway enrichment analysis across The Cancer Genome Atlas (TCGA) cohort.</p><p><strong>Results: </strong>SLC39A14 was found to be significantly upregulated across multiple tumor types and associated with a poor prognosis, immune-stromal infiltration, and ferroptosis resistance. Among all cancer types analyzed, glioblastoma multiforme (GBM) and kidney renal cell carcinoma (KIRC) exhibited the significantly prognostic associations and the most pronounced differential expression of SLC39A14. Single-cell analysis revealed that SLC39A14 expression was enriched between stromal and immune populations, hypoxic perivascular niches, confirming its microenvironment-specific functions. These findings were corroborated by DNA methylation data showing promoter hypomethylation of SLC39A14 in tumors compared to normal tissues. Functionally, SLC39A14 was highly enriched in pathways related to angiogenesis, the epithelial-to-mesenchymal transition, cytokine signaling, and oxidative stress adaptation including vascular endothelial growth factor (VEGF) and cell metabolism-related signaling. A nomogram integrating SLC39A14 expression with clinical parameters improved overall survival predictions.</p><p><strong>Conclusions: </strong>In this study, we identified SLC39A14 as a dual regulator at the interface of ferroptosis and glycosylation, with significant impacts on tumor microenvironmental remodeling and therapeutic resistance. By leveraging multi-omics and single-cell transcriptomic data, we establish SLC39A14 as a promising prognostic biomarker and therapeutic target, particularly in brain and kidney cancers where ferroptosis modulation could offer novel clinical strategies.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"363"},"PeriodicalIF":6.0,"publicationDate":"2025-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145343595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NR2F6 regulates Temozolomide resistance in glioma via the E2F2-PARP1 pathway.","authors":"Bo Wang, Pengfei Xue, Rongrong Li, Yaxin Liang, Zhaohao Wang, Lili Yan, Qianqian Zhang, Conghui Tian, Lili Yi, Cuncun Yang, Xin Li, Juan Zheng","doi":"10.1186/s12935-025-03986-6","DOIUrl":"https://doi.org/10.1186/s12935-025-03986-6","url":null,"abstract":"<p><strong>Background: </strong>Glioma is the most common primary malignant brain tumor in adults. Temozolomide (TMZ) represents a standard-of-care chemotherapeutic agent in glioblastoma (GBM). However, the development of drug resistance constitutes a significant hurdle in the treatment of malignant glioma. Elucidating the mechanisms of temozolomide (TMZ) resistance in glioma is of critical clinical importance for improving patient prognosis and developing novel therapeutic strategies.</p><p><strong>Methods: </strong>We obtained RNA sequencing (RNA-seq) data of 648 glioma samples from The Cancer Genome Atlas (TCGA) and 325 samples from the Chinese Glioma Genome Atlas (CGGA) as study cohorts. Additionally, we validated the expression characteristics of the NR2F6 gene in our in-house cohort of glioma patients. Furthermore, we investigated the potential mechanism of NR2F6 in TMZ resistance in glioma by constructing TMZ-resistant cell lines in vitro. Statistical analyses and graphical work were primarily performed using R language and GraphPad Prism software.</p><p><strong>Results: </strong>We observed a significant upregulation of NR2F6 expression in high-grade gliomas, which is associated with an unfavorable prognosis in patients. Concurrently, our findings revealed a significant upregulation of NR2F6 in drug-resistant cells, which induced TMZ resistance in glioma cells via the E2F2-PARP1 axis.</p><p><strong>Conclusion: </strong>In brief, NR2F6, as a nuclear transcription factor, enhances the transcription of E2F2.The increased expression of E2F2 enhances PARP1 expression, which in turn facilitates TMZ-mediated DNA damage repair, thereby diminishing glioma sensitivity to TMZ.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"366"},"PeriodicalIF":6.0,"publicationDate":"2025-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145343548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis and non-coding RNAs in lung cancer: exploring molecular mechanisms and diagnostic/therapeutic implications.","authors":"Hedong Xue, Melika Malek, Liangyu Li","doi":"10.1186/s12935-025-03949-x","DOIUrl":"https://doi.org/10.1186/s12935-025-03949-x","url":null,"abstract":"<p><p>Lung cancer is the second most prevalent type of cancer on a global scale, and is widely known for being the deadliest. Revealing the fundamental molecular mechanisms of this condition has the potential to unlock fresh possibilities and avenues for managing it. Ferroptosis is a newly discovered type of controlled cell death that distinguishes itself from traditional forms of programmed cell death, specifically apoptosis and necrosis, through its distinct biochemical and structural characteristics. Changes made to the mechanism that regulates ferroptosis can have a significant influence on the development of various illnesses, such as, though not limited to, lung cancer. Based on scientific studies, it has been proven that cancer cells possess a significant capability to inhibit ferroptosis, leading to their continuous growth and survival. The presence of non-coding RNAs has a profound influence on controlling a wide range of cellular functions, with a particular focus on cancer. They have been closely associated with all key features of lung cancer. Fresh findings have indicated that these particles also have the task of controlling ferroptosis. Thus, the use of non-coding RNA as a therapeutic strategy offers a potentially effective option for regulating ferroptosis in the management of cancer. The main focus of this overview is on ncRNAs and their function in controlling ferroptosis, specifically within the context of lung cancer.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"364"},"PeriodicalIF":6.0,"publicationDate":"2025-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145343518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PMA exerts anti-leukemia effect in Ph⁺ ALL through activating PKC δ and its down-stream molecules.","authors":"Xu Wang, Jinfeng Tan, Jie Tang, Teng Wang, Dachuan Zeng, Renren Zheng, Jing Hu, Suotian Liu, Wei Wei, Jie Zou, Yan Du, Zhenglan Huang, Miao Gao","doi":"10.1186/s12935-025-04013-4","DOIUrl":"https://doi.org/10.1186/s12935-025-04013-4","url":null,"abstract":"<p><strong>Background: </strong>Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph⁺ ALL) is a subtype of precursor B ALL in genetics and is recognized as a subclass with poor prognosis. Tyrosine kinase inhibitors (TKIs) greatly improve the prognosis of Ph⁺ ALL patients. However, the long-term survival rate is still low (with a 3-year survival rate only 55%). Hence, it is urgent to explore new therapies to improve prognosis for Ph⁺ ALL patients. Protein kinase C (PKC) is proven to be a tumor suppressor in recent years. Activation of PKC by its novel agonist PMA reverts the malignancy of many hematological diseases. However, the effect of PMA on Ph⁺ ALL is unclear.</p><p><strong>Methods: </strong>We investigated the biological effects of PMA on Ph⁺ ALL cells and the potential mechanism in this study. In this study, the SUP-B15 and BP190 cell lines were subjected to PMA treatment. Cell proliferation, cycle distribution, apoptosis, protein expression levels, and gene expression changes were assessed using CCK-8 assay, flow cytometry, Western blot analysis, DAPI staining, and quantitative real-time PCR. Additionally, bone marrow mononuclear cells were isolated for further investigation, and RNA sequencing was conducted on SUP-B15 cells. Furthermore, the mouse model was established to evaluate the in vivo biological effects of PMA.</p><p><strong>Results: </strong>We found that PMA could promote apoptosis, inhibit proliferation and promote differentiation of human Ph⁺ ALL cells. More importantly, we demonstrated for the first time that these effects caused by PMA were related to the activation of PKC δ and its down-stream molecules, such as p-ERK, p21 and so on.</p><p><strong>Conclusions: </strong>PMA exerts an anti-leukemia effect in Ph⁺ ALL by activating PKC δ and its downstream molecules, thereby demonstrating its potential as a therapeutic agent for Ph⁺ ALL.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"365"},"PeriodicalIF":6.0,"publicationDate":"2025-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145343596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Suppression of pentraxin 3 inhibits human osteosarcoma cell metastasis by repressing MAZ through STAT3 pathway.","authors":"Chia-Hsuan Chou, Yi-Hsien Hsieh, Pei-Ni Chen, Jia-Sin Yang, Chih-Hsin Tang, Shun-Fa Yang, Ko-Hsiu Lu","doi":"10.1186/s12935-025-04008-1","DOIUrl":"10.1186/s12935-025-04008-1","url":null,"abstract":"","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"359"},"PeriodicalIF":6.0,"publicationDate":"2025-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12535031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145312484","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}