Journal of Experimental & Clinical Cancer Research最新文献

{"title":"JNK pathway suppression mediates insensitivity to combination endocrine therapy and CDK4/6 inhibition in ER+ breast cancer.","authors":"Sarah Alexandrou, Christine S Lee, Kristine J Fernandez, Celine E Wiharja, Leila Eshraghi, John Reeves, Daniel A Reed, Neil Portman, Zoe Phan, Heloisa H Milioli, Iva Nikolic, Antonia L Cadell, David R Croucher, Kaylene J Simpson, Elgene Lim, Theresa E Hickey, Ewan K A Millar, Carla L Alves, Henrik J Ditzel, C Elizabeth Caldon","doi":"10.1186/s13046-025-03466-9","DOIUrl":"10.1186/s13046-025-03466-9","url":null,"abstract":"<p><p>CDK4/6 inhibitors in combination with endocrine therapy are now used as front-line treatment for patients with estrogen-receptor positive (ER+) breast cancer. While this combination improves overall survival, the mechanisms of disease progression remain poorly understood. Here, we performed unbiased genome-wide CRISPR/Cas9 knockout screens using endocrine sensitive ER+ breast cancer cells to identify novel drivers of resistance to combination endocrine therapy (tamoxifen) and CDK4/6 inhibitor (palbociclib) treatment. Our screens identified the inactivation of JNK signalling, including loss of the kinase MAP2K7, as a key driver of drug insensitivity. We developed multiple CRISPR/Cas9 knockout ER+ breast cancer cell lines (MCF-7 and T-47D) to investigate the effects of MAP2K7 and downstream MAPK8 and MAPK9 loss. MAP2K7 knockout increased metastatic burden in vivo and led to impaired JNK-mediated stress responses, as well as promoting cell survival and reducing senescence entry following endocrine therapy and CDK4/6 inhibitor treatment. Mechanistically, this occurred via loss of the AP-1 transcription factor c-JUN, leading to an attenuated response to combination endocrine therapy plus CDK4/6 inhibition. Furthermore, analysis of clinical datasets found that inactivation of the JNK pathway was associated with increased metastatic burden, and low pJNK^T183/Y185 activity correlated with a poorer response to systemic endocrine and CDK4/6 inhibitor therapies in both early-stage and metastatic ER+ breast cancer cohorts. Overall, we demonstrate that suppression of JNK signalling enables persistent growth during combined endocrine therapy and CDK4/6 inhibition. Our data provides the pre-clinical rationale to stratify patients based on JNK pathway activity prior to receiving combination endocrine therapy and CDK4/6 inhibition.</p>","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":"44 1","pages":"244"},"PeriodicalIF":12.8,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12363127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144876552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"COL10A1⁺ fibroblasts promote colorectal cancer metastasis and M2 macrophage polarization with pan-cancer relevance.","authors":"Shangshang Hu, Muzi Ding, Jinwei Lou, Jian Qin, Yuhan Chen, Zixuan Liu, Yue Li, Junjie Nie, Mu Xu, Huiling Sun, Xinliang Gu, Tao Xu, Shukui Wang, Shukui Wang, Yuqin Pan","doi":"10.1186/s13046-025-03510-8","DOIUrl":"10.1186/s13046-025-03510-8","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) is a common gastrointestinal cancer with poor response to therapy and high metastatic risk. Cancer-associated fibroblasts (CAFs) support tumor progression, but their functional heterogeneity remains poorly understood.</p><p><strong>Methods: </strong>We integrated multi-omics data from 10,164 samples, including single-cell, bulk, spatial transcriptomics, and proteomics, to identify and characterize CAF subpopulations. Functional validation was performed using molecular assays, in vivo models, and drug screening.</p><p><strong>Results: </strong>We identified a COL10A1-positive fibroblast subpopulation (COL10A1⁺Fib) associated with CRC progression and poor patient prognosis. COL10A1⁺Fib promotes tumor cell proliferation, immune suppression, and metastasis. Mechanistically, COL10A1⁺Fib facilitates epithelial-mesenchymal transition (EMT) in CRC cells via COL10A1 secretion and induces M2 macrophage polarization through the COL10A1/CD18/JAK1/STAT3 signaling axis. In turn, M2 macrophages enhance COL10A1 expression in fibroblasts via the TGF-β/RUNX2 pathway, forming a pro-tumorigenic feedback loop. The DNA-PKcs inhibitor NU7441 reduces COL10A1 expression, suppresses CAF activity, and reverses EMT and M2 polarization. Pan-cancer analysis suggests that COL10A1⁺Fib may have similar functional roles across multiple major solid tumors.</p><p><strong>Conclusion: </strong>Our study identifies a CAF subpopulation, COL10A1⁺Fib, associated with CRC progression and immune suppression, suggesting it as a potential therapeutic target in CRC and possibly other malignancies.</p>","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":"44 1","pages":"243"},"PeriodicalIF":12.8,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12360028/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144876551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRIM6 ablation reverses ICB resistance in MSS gastric cancer by unleashing cGAS-STING-dependent antitumor immunity.","authors":"Yinan Niu, Chen Ding, Quansheng Wang, Jingyi Yin, Lingmeng Li, Wenshuai Liu, Xuefei Wang, Liyu Huang","doi":"10.1186/s13046-025-03513-5","DOIUrl":"10.1186/s13046-025-03513-5","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancers are classified into four molecular subtypes according to The Cancer Genome Atlas (TCGA) classification: Epstein-Barr virus-positive (EBV-positive), microsatellite instability-high (MSI-H), chromosomal instability (CIN), and genomically stable (GS). Unlike MSI-H gastric cancer, GS and CIN subtypes exhibit immunologically inert microenvironments and demonstrate minimal response to immune checkpoint blockade (ICB), necessitating novel strategies to overcome immunotherapy resistance.</p><p><strong>Methods: </strong>Through weighted gene co-expression network analysis (WGCNA), we identified the E3 ubiquitin ligase TRIM6 as inversely associated with MSI-H status. TRIM6-knockout murine models and subcutaneous tumors were subjected to flow cytometry, RNA sequencing, immunoblotting, and ubiquitination assays to characterize tumor-infiltrating lymphocytes (TILs), pathway activation, and TRIM6-mediated regulation of the cGAS-STING axis.</p><p><strong>Results: </strong>Hypermethylation-mediated TRIM6 downregulation distinguished MSI-H from microsatellite stable (MSS) gastric cancers. Clinically, TRIM6 expression inversely correlated with cytotoxic T lymphocyte (CTL) infiltration and anti-PD-1/PD-L1 therapeutic efficacy. Mechanistically, TRIM6 catalyzed K27-linked polyubiquitination of cGAS, triggering its proteasomal degradation and consequent suppression of the cGAS-STING pathway. TRIM6 ablation enhanced CD8⁺ T lymphocytes infiltration via cGAS-mediated innate immune response and synergized with anti-PD-L1 therapy in MSS gastric tumors.</p><p><strong>Conclusions: </strong>Our results elucidate TRIM6-mediated suppression of antitumor immunity as a novel mechanism underlying ICB resistance in MSS gastric cancer, positioning TRIM6 as both a predictive biomarker and therapeutic target for immunologically cold subtypes.</p>","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":"44 1","pages":"242"},"PeriodicalIF":12.8,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12355757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144859861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial expression of concern: ERRα suppression enhances the cytotoxicity of the MEK inhibitor trametinib against colon cancer cells.","authors":"Sheng Zhou, Hongwei Xia, Huanji Xu, Qiulin Tang, Yongzhan Nie, Qi Yong Gong, Feng Bi","doi":"10.1186/s13046-025-03507-3","DOIUrl":"10.1186/s13046-025-03507-3","url":null,"abstract":"","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":"44 1","pages":"241"},"PeriodicalIF":12.8,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12355848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144856869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-7 inhibits progression of glioblastoma by impairing autophagy resolution, energy metabolism and ECM remodeling.","authors":"Marta Torrecilla-Parra, Virginia Pardo-Marqués, Antonio C Fuentes-Fayos, Miguel E G-García, Mario Fernández-de Frutos, José L López-Aceituno, Cristina Puigdueta, Carmen Zamora, Ana Pérez-García, Juan F Aranda, Rebeca Busto, Manuel D Gahete, Raúl M Luque, Cristina M Ramírez","doi":"10.1186/s13046-025-03504-6","DOIUrl":"10.1186/s13046-025-03504-6","url":null,"abstract":"<p><strong>Background: </strong>Due to the poor prognosis of patients suffering malignant brain tumors such as glioblastoma multiforme (GBM), the search for new therapeutic strategies with more efficacy and higher survival rate is of utmost urgency. Growing evidence suggests that alterations in autophagy and metabolism critically contribute to the pathogenesis and progression of GBM. In this context, microRNAs are known to regulate autophagy and associated cellular functions, which point them as promising therapeutic candidates. We previously established the role of miR-7 in regulating relevant metabolic pathways related to insulin signaling and cholesterol homeostasis.</p><p><strong>Methods: </strong>Bioinformatics analysis was performed to identify miR-7 target genes potentially involved in the regulation of metabolism and cellular processes related to GBM. Ectopic expression of miR-7 was assessed to investigate its role in macroautophagy and energy metabolism. In vivo, miR-7 levels were restored in a mouse GBM xenograft model to evaluate its potential therapeutic effect in already established tumors. Additional mechanistic approaches, including transcriptomics, bioinformatics, and histopathological analyses, indicate that miR-7 modifies the tumor phenotype by altering key genes involved in extracellular matrix (ECM) remodeling in vivo.</p><p><strong>Results: </strong>Herein, we unveiled new conceptual and functional pathophysiological avenues in GBM, with potential therapeutic implications, by demonstrating a novel dual role of miR-7 on the regulation of metabolism, through the impairment of the mitochondrial function and glycolysis, and autophagy, by inducing the initiation process through the regulation of PI3K/AKT/mTORC1 signaling, while blocking later stages via posttranscriptional inhibition of two key SNARE proteins, STX17 and SNAP29. Furthermore, in vivo studies using a preclinical model showed that miR-7 overexpression in already established GBM tumors promotes a significant inhibition of tumor size and progression and replicates the metabolic defects found in vitro. Moreover, our novel findings indicate that miR-7 modifies the tumor phenotype by promoting alterations in its mechanism of extracellular matrix remodeling in vivo.</p><p><strong>Conclusion: </strong>Altogether, our study provides solid, convincing evidence demonstrating that miR-7 might be used as a promising therapeutic target for GBM, paving the way to explore its potential as novel biomarker and actionable target candidate for this lethal cancer.</p>","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":"44 1","pages":"237"},"PeriodicalIF":12.8,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144856871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRP channels and cancer modulation: a voyage beyond metabolic reprogramming, oxidative stress and the advent of nanotechnologies in targeted therapy.","authors":"Marialaura Giannaccari, Chiara Florindi, Nora Bloise, Francesco Moccia, Francesco Lodola, Livia Visai","doi":"10.1186/s13046-025-03495-4","DOIUrl":"10.1186/s13046-025-03495-4","url":null,"abstract":"<p><p>Transient receptor potential (TRP) channels are a large family of non-selective cation channels that play critical roles in cellular homeostasis and signal transduction. Recent investigations have clearly highlighted their involvement in cancer biology, particularly in the regulation of cancer metabolism. Unlike normal cells, cancer cells tend to favour the energy inefficient glycolytic pathway over the more effective oxidative phosphorylation process. TRP channels are involved in critical steps of cancer-related metabolic reprogramming by influencing intracellular Ca²⁺ signaling. Their dysregulation can intensify oxidative stress, thereby promoting oncogenic transformation and tumor progression. The intricate interplay between TRP channels, metabolic reprogramming and oxidative stress promotes cancer cell progression and resistance to treatment. This review highlights the crucial role of TRP channels in tumorigenesis. It examines how TRPM7 and TRPM8 contribute to metabolic reprogramming by its involvement in glycolysis pathway. Additionally, it explores the involvement of TRPML1, TRPA1, TRPM2, and TRPV1 in modulating reactive oxygen species (ROS) levels within cancer cells, analyzing the ROS dual role in tumor modulation. The advent of nanotechnology, particularly through the utilisation of engineered nanoparticles, has facilitated the selective modulation of TRPA1, TRPM2, and TRPV1 channels. This technological breakthrough has paved the way for novel and more targeted anticancer treatment strategies. The integration of molecular insights with cutting-edge technological approaches holds great promise for the development of more effective and targeted cancer treatments.</p>","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":"44 1","pages":"240"},"PeriodicalIF":12.8,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351952/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144856873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tfcp2l1 as a central integrator of hypoxia, dedifferentiation, and tumor progression.","authors":"Cynthia Clemente-González, Amancio Carnero","doi":"10.1186/s13046-025-03501-9","DOIUrl":"10.1186/s13046-025-03501-9","url":null,"abstract":"","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":"44 1","pages":"236"},"PeriodicalIF":12.8,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351891/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144856872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Arginine depletion potentiates standard-of-care chemo-immunotherapy in preclinical models of high-risk neuroblastoma.","authors":"Kimberley M Hanssen, Jayne Murray, Ruby Pandher, Stephanie Alfred, Laura D Gamble, Jennifer Brand, Erin Mosmann, Frances K Kusuma, Crystal Mak, Adam Kearns, Alvin Kamili, Caroline Atkinson, Alexis Z Minchaca, Jean Bertoldo, David S Ziegler, Francis Mussai, Paul N M Cheng, Murray D Norris, Jamie I Fletcher, Michelle Haber","doi":"10.1186/s13046-025-03502-8","DOIUrl":"10.1186/s13046-025-03502-8","url":null,"abstract":"<p><strong>Background: </strong>Dysregulated amino acid metabolism creates cancer-specific vulnerabilities. Neuroblastoma tumors have dysregulated arginine metabolism that renders them sensitive to systemic arginine deprivation. Arginase therapy has been proposed as a therapeutic approach for neuroblastoma treatment and has a favorable safety profile in pediatric cancer patients, however optimal therapeutic combinations remain unexplored.</p><p><strong>Methods: </strong>The anti-tumor effects of BCT-100, a pegylated human arginase, were studied in neuroblastoma cell models by metabolite profiling, proteomics, and viability, clonogenicity, and protein translation assays. BCT-100 efficacy was assessed in the Th-MYCN transgenic neuroblastoma mouse model and in neuroblastoma cell line and patient-derived xenograft models.</p><p><strong>Results: </strong>In vitro, depletion of arginine by BCT-100 arrested protein translation and cellular proliferation, with effects on clonogenicity enhanced in combination with standard-of-care chemotherapeutics SN-38/temozolomide and mafosfamide/topotecan. In vivo, BCT-100 treatment spared liver arginine while significantly depleting plasma and tumor arginine in Th-MYCN mice, and extended tumor latency (> 100 vs. 45.5 days) in mice pre-emptively treated at weaning. In mice with established tumors, BCT-100 prolonged tumor progression delay when combined with standard-of-care chemo- (> 90 vs. 25 days) or chemo-immuno-therapy (49.5 vs. 35.5 days). Tumor progression delay was also observed in cell line and patient-derived xenografts with BCT-100 treatment, including relapsed/refractory disease models. No increased toxicity was observed with the addition of BCT-100 to established therapies.</p><p><strong>Conclusions: </strong>The arginase BCT-100 profoundly disrupts neuroblastoma growth in vitro and in vivo, an effect enhanced in combination with standard-of-care chemo-immuno-therapy. Our data supports further assessment of arginine-depleting combination therapies as a new treatment strategy for neuroblastoma.</p>","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":"44 1","pages":"239"},"PeriodicalIF":12.8,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144856868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HAS1^high cancer associated fibroblasts located at the tumor invasion front zone promote oral squamous cell carcinoma invasion via ECM remodeling.","authors":"Wanyong Jin, Qiuya Yu, Liyuan Yu, Ting Zhou, Xiren Wang, Wanqiu Lu, Xiaoxin Zhang, Liang Ding, Qingang Hu, Yanhong Ni","doi":"10.1186/s13046-025-03493-6","DOIUrl":"10.1186/s13046-025-03493-6","url":null,"abstract":"<p><strong>Background: </strong>Although tumor cell heterogeneity between the tumor center (TC) and invasion front (IF) of oral squamous cell carcinoma (OSCC) is well documented, the morphological, molecular, and functional characteristics of cancer-associated fibroblasts (CAFs) in these regions remain poorly understood.</p><p><strong>Methods: </strong>We examined hematoxylin and eosin (H&E)-stained OSCC sections to assess CAF morphology and correlation with patient prognosis. We then isolated paired CAFs from the tumor center (CAF^TC) and invasion front (CAF^IF) of four OSCC patients and compared their ECM-remodeling activity and pro-tumorigenic effects on OSCC cells. Furthermore, RNA sequencing identified differentially expressed genes between CAF^TC and CAF^IF. Finally, based on RNA-seq findings, we knocked down hyaluronan synthase 1 (HAS1) in CAF^IF to evaluate its role in extracellular matrix (ECM) remodeling and tumor invasion.</p><p><strong>Results: </strong>Compared to CAF^TC, CAF^IF exhibited a plump cell morphology and were associated with shorter disease-free survival. Functionally, CAF^IF showed higher ECM-remodeling activity and more effective ability for promoting OSCC invasion and lymph node metastasis than CAF^TC. RNA-seq identified HAS1 was significantly upregulated in CAF^IF, promoting hyaluronic acid (HA) production and ECM remodeling. HAS1 knockdown in CAF^IF diminished ECM remodeling and attenuated the ability of CAF^IF to promoting OSCC invasion.</p><p><strong>Conclusion: </strong>CAF^IF with plump cell morphology showed pro-invasive abilities, driven in part by HAS1 overexpression and ECM remodeling, suggesting that targeting HAS1-driven ECM remodeling could be a promising therapeutic strategy.</p>","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":"44 1","pages":"238"},"PeriodicalIF":12.8,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12351772/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144856870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Circular RNA circ-CPA4/ let-7 miRNA/PD-L1 axis regulates cell growth, stemness, drug resistance and immune evasion in non-small cell lung cancer (NSCLC).","authors":"Weijun Hong, Min Xue, Jun Jiang, Yajuan Zhang, Xiwen Gao","doi":"10.1186/s13046-025-03499-0","DOIUrl":"10.1186/s13046-025-03499-0","url":null,"abstract":"","PeriodicalId":50199,"journal":{"name":"Journal of Experimental & Clinical Cancer Research","volume":"44 1","pages":"235"},"PeriodicalIF":12.8,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12341128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144838461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}