Cancer Cell International最新文献

{"title":"Role of S1PR1 in VEGF-exosomes mediated resistance of hepatocellular carcinoma to anti-angiogenesis therapy.","authors":"Xinghong Yao, Min Tang, Liang Li, Ye Zeng","doi":"10.1186/s12935-025-03907-7","DOIUrl":"https://doi.org/10.1186/s12935-025-03907-7","url":null,"abstract":"<p><strong>Background: </strong>Anti-angiogenesis therapy (AAT) triggers vascular endothelial growth factor (VEGF)-exosomes secretion from tumor-associated endothelial cells (TAECs) for hepatocellular carcinoma (HCC) tubulogenesis and metastasis. Sphingosine-1-phosphate receptor 1 (S1PR1) has been implicated in HCC progression, but it was targeted by microRNA-9 (miR-9) that might mediate the formation of TAECs. This study aims to investigate the role of miR-9 and VEGF-exosomes in S1PR1-mediated HCC progression and resistance to AAT.</p><p><strong>Methods: </strong>The expression and distribution of miR-9 in HCC tissues were analyzed using qRT-PCR and fluorescence in situ hybridization (FISH). The impact of S1PR1 knockdown on VEGF-exosome uptake, as well as miR-9 and VEGF-exosome-induced epithelial-mesenchymal transition (EMT), migration, and invasion of HCC cells, was assessed by Transwell assays, fluorescence microscopy, and Western blotting.</p><p><strong>Results: </strong>miR-9 expression was significantly upregulated in HCC tissues and selectively localized in CD34⁺ endothelial cells within paracancerous microvessels, suggesting its role in TAEC transformation.miR-9 promoted EMT and enhanced HCC cell migration and invasion, effects that were further potentiated by VEGF-exosomes. S1PR1 knockdown significantly inhibited VEGF-exosome uptake and suppressed miR-9- and VEGF-exosome-induced EMT, migration, and invasion of HCC cells.</p><p><strong>Conclusion: </strong>In conclusion, miR-9 facilitates HCC progression by enhancing tumor malignancy and promoting AAT resistance through TAEC-mediated VEGF-exosome secretion. S1PR1 is a critical mediator of this process, and its inhibition represents a potential therapeutic strategy to overcome AAT resistance in HCC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"264"},"PeriodicalIF":5.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648663","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":"EIF4A3-induced circPRKAR1B promotes esophageal squamous cell carcinoma progression through binding PKM2 to regulate NF-κB induced CCL3 secretion.","authors":"Shiji Li, Junji Ma, Wenxiu Jia, Yangyang Duan, Jingran Wang, Xiuning Zhang, Yan Han","doi":"10.1186/s12935-025-03905-9","DOIUrl":"https://doi.org/10.1186/s12935-025-03905-9","url":null,"abstract":"<p><p>Esophageal squamous cell carcinoma (ESCC) ranks as the sixth leading cause of cancer-related deaths globally, with over half of these cases occurring in China. However, the underlying molecular mechanisms of this disease are still not fully elucidated. Numerous circular RNAs (circRNAs) have been implicated in the initiation and progression of malignant tumors through diverse molecular pathways. Nevertheless, the clinical significance and functional roles of the majority of circRNAs associated with ESCC progression remain inadequately characterized. In the present study, we identified a novel circular RNA, designated as circPRKAR1B, which was found to be upregulated in esophageal squamous cell carcinoma (ESCC) tissues and associated with poor prognosis in ESCC patients. Functionally, the overexpression of circPRKAR1B enhanced the proliferation and invasive capabilities of ESCC cells. Mechanistically, circPRKAR1B facilitates the progression of ESCC by interacting with PKM2, which in turn activates the NF-κB signaling pathway, thereby promoting the secretion of CCL3. Additionally, EIF4A3 promotes the expression of circPRKAR1B by binding to its downstream flanking sequences. These findings reveal a previously unrecognized role of circular RNA in the progression of ESCC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"262"},"PeriodicalIF":5.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648660","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":"Identification and evaluation of metabolic mRNAs and key miRNAs in colorectal cancer liver metastasis.","authors":"Guanxuan Chen, Shiwen Wang, Meng Zhang, Wenna Shi, Ruoyu Wang, Wanqi Zhu","doi":"10.1186/s12935-025-03903-x","DOIUrl":"https://doi.org/10.1186/s12935-025-03903-x","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) represents a major global health challenge due to its high lethality, largely attributable to liver metastasis. Despite the established correlation between metabolic reprogramming of cancer cells and their proliferation, invasion, and metastasis, the specific role of metabolism-associated mRNAs in the liver metastasis of CRC remains unelucidated.</p><p><strong>Methods: </strong>In our research, we procured and analyzed CRC liver metastasis-associated datasets from the GEO database. Subsequently, we employed Weighted Gene Co-expression Network Analysis (WGCNA) to construct an integrated co-expression network of mRNAs and miRNAs, facilitating the identification of pivotal mRNAs and miRNAs. We screened the featured genes using a machine-learning technique, followed by an evaluation of their diagnostic potential for CRC liver metastasis. Additionally, we conducted a functional enrichment analysis and constructed a network of miRNA-targeted mRNAs. Lastly, leveraging the UCSC Xena database, we assessed the correlation between core mRNAs and the clinical attributes and prognosis of CRC patients. Clinical samples from CRC patients and healthy volunteers were collected for validation using qRT-PCR.</p><p><strong>Results: </strong>Our study identified 12 mRNAs and 4 miRNAs significantly associated with CRC liver metastasis. Functional enrichment analysis indicated that these key genes were intricately linked with biological processes like lipid transport, homeostasis, and metabolism. By implementing LASSO and SVM algorithms, we pinpointed six core mRNAs from the key mRNAs. Their expression patterns and diagnostic performance were validated across multiple datasets. Particularly, CAV1 showed significant diagnostic performance to discern between CRC and CRC liver metastasis samples. Additionally, we discerned two key miRNAs (hsa-miR-1246 and hsa-miR-1290) exhibiting diagnostic performance. Lastly, our findings indicate a significant association between AGT, FABP4, and GPD1L and the prognosis of CRC patients with liver metastasis. PCR validation in 40 paired tissue samples showed downregulation of CAV1 and upregulation of miRNA-1290 in CRC tissues of patients with liver metastasis.</p><p><strong>Conclusions: </strong>This investigation identified modular genes and miRNAs linked to CRC liver metastasis, along with metabolism-associated differentially expressed mRNAs. These pivotal mRNAs and miRNAs could be instrumental in elucidating the biological mechanisms underpinning CRC liver metastasis and suggesting candidate biomarkers.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"265"},"PeriodicalIF":5.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648661","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":"Medicinal plants: nutritional, immunological and therapeutic role in treating cancer-related malnutrition: a comprehensive review.","authors":"Mohamed T El-Saadony, Samar Sami Alkafaas, Ahmed M Saad, Dina Mostafa Mohammed, Sameh A Korma, Heba M Salem, Taia A Abd El-Mageed, Mohamed I Elsalahaty, Sara Samy Elkafas, Walid F A Mosa, Ahmed Ezzat Ahmed, Essam H Ibrahim, Fawze Alnadari, Betty T Mathew, Alaa S Abdelhamid, Sahar F Allaban, Samah A Loutfy, Soumya Ghosh, Hanya Y Assal, Marawan K El-Tarabily, Synan F AbuQamar, Khaled A El-Tarabily","doi":"10.1186/s12935-025-03720-2","DOIUrl":"https://doi.org/10.1186/s12935-025-03720-2","url":null,"abstract":"<p><p>Cancer is the second leading cause of death globally, following microbial infection, with an estimated 16 million deaths projected by 2040. However, natural resources can potentially treat up to 60% of cancer cases. Various cancers, including those affecting the breast, prostate, stomach, colon, lung, liver, kidney, bone, skin, and blood, have strong dietary connections regarding their occurrence and prevention. Cancer and its treatments, particularly chemotherapy, are closely associated with malnutrition in humans. The adverse effects of medical therapies and the disease itself often prevent patients with cancer from meeting their nutritional needs through regular food intake. The etiology of malnutrition in patients with cancer is complex and multifactorial, influenced by the type and location of cancer, disease stage, side effects of treatment, economic status, functional capacity, symptoms impacting nutrition, fasting requirements, inadequate dietary therapy, and awareness of the clinical staff regarding the role of dietary habits in diagnosis, treatment, and quality of life. Although there have been advances in drug-targeted therapies, they remain unelucidated, and therefore, this review aims to elucidate the relationship between cancer, chemical treatments, and malnutrition. In addition, it highlights the significant role of medicinal plants in treating various cancers and mitigating the adverse side effects of chemotherapy, offering a comprehensive understanding of their nutritional, immunological, and therapeutic benefits.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"266"},"PeriodicalIF":5.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648662","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":"A LINC00472-encoded polypeptide impedes migration and proliferation through modulation of the HDAC2/SP1 axis in non-small cell lung cancer cells.","authors":"Lei Xu, Haoyong Kuang, Haodong Peng, Sen Wu, Yu Bai, Xiangbo Jia, Wenjian Yao","doi":"10.1186/s12935-025-03901-z","DOIUrl":"https://doi.org/10.1186/s12935-025-03901-z","url":null,"abstract":"<p><strong>Objective: </strong>While long non-coding RNAs (lncRNAs) are increasingly recognized as sources of functional micropeptides, their roles in non-small cell lung cancer (NSCLC) remain poorly characterized. This study investigates the therapeutic potential and molecular mechanism of LINC00472-encoded polypeptide in NSCLC.</p><p><strong>Methods: </strong>Through integration of ribosome profiling, transcriptomics, and co-expression analysis, we systematically identified lncRNA-encoded polypeptides in NSCLC. Translational competence was validated via ribosome affinity purification (TRAP), Western blot, and immunofluorescence (IF). Functional assays (CCK-8, EdU, wound healing, transwell) and xenograft models assessed anti-tumor effects. HDAC2/SP1 interaction dynamics were analyzed by co-IP and luciferase reporter systems.</p><p><strong>Results: </strong>Multi-omics screening identified LINC00472 as a bifunctional transcript encoding a 15-aa polypeptide (LINC00472-ORF). LINC00472-ORF exhibited potent tumor-suppressive activity, reducing NSCLC proliferation and motility in vitro, while suppressing xenograft growth in vivo. Mechanistically, LINC00472-ORF disrupted HDAC2/SP1 interaction, inducing SP1 hyperacetylation, cytoplasmic retention, and transcriptional inactivation of downstream oncogenic genes.</p><p><strong>Conclusion: </strong>We unveil LINC00472-ORF as a dual-function therapeutic agent that targets the HDAC2/SP1 axis to inhibit NSCLC progression.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"263"},"PeriodicalIF":5.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648659","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":"Stromal PLAU mediates tumor progression and informs a novel therapeutic target in triple-negative breast cancer.","authors":"Jun Zou, Jingyao Zhang, Yu Li, Baowen Yuan, Yuanyi Wang, Yalong Qi, Qian Wang, Wan Qin, Xianglin Yuan, Binghe Xu","doi":"10.1186/s12935-025-03867-y","DOIUrl":"10.1186/s12935-025-03867-y","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is an aggressive subtype characterized by limited treatment options and poor prognosis. Recent evidence highlights the crucial role of cancer-associated fibroblasts (CAFs) in TNBC progression, yet their molecular characteristics remain incompletely understood. In this study, we performed a comprehensive analysis combining bioinformatics approaches with experimental validation to investigate CAF-related genes in TNBC. Using weighted gene co-expression network analysis (WGCNA) of TNBC samples from TCGA and METABRIC datasets, we identified 185 CAF-related genes significantly associated with extracellular matrix organization and TGF-β signaling pathways. Through rigorous statistical modeling, we developed a 3-gene prognostic signature (CERCAM, JAM3, PLAU) that effectively stratified TNBC patients into high- and low-risk groups with distinct survival outcomes. Importantly, we validated the functional role of PLAU, one of the signature genes, through in vitro and in vivo experiments. Results showed that CAF-derived PLAU played key role in the malignant behaviors of TNBC. Our findings provide new insights into CAF-mediated TNBC progression and suggest potential stromal targets for therapeutic intervention.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"259"},"PeriodicalIF":5.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12255126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616324","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":"A multi-analyte liquid biopsy approach for nonseminomatous testicular germ cell tumors: combining cfDNA and N-glycan analysis in blood and seminal plasma.","authors":"Jure Krasic, Dinko Soic, Lucija Skara Abramovic, Ivona Kolosnjaj, Miroslav Tomic, Alen Vrtaric, Sasa Kralik Oguic, Nina Gelo, Ana Katusic Bojanac, Davor Jezek, Dinko Mitrecic, Monika Ulamec, Tomislav Kulis, Olga Gornik, Nino Sincic","doi":"10.1186/s12935-025-03887-8","DOIUrl":"10.1186/s12935-025-03887-8","url":null,"abstract":"<p><strong>Background: </strong>Nonseminomatous testicular germ cell tumors (NSE) present significant diagnostic challenges, especially for the early detection of serum tumor marker (STM) negative cases. Current diagnostic tools are limited, highlighting the need for innovative approaches. This study investigates a novel multi-analyte approach combining circulating cell-free DNA (cfDNA) and N-glycan profiling in both blood and seminal plasma to improve NSE diagnostics.</p><p><strong>Methods: </strong>The study included 41 NSE patients and 114 healthy controls. Diagnostic potential of cfDNA parameters (quality and fragmentation), cfDNA methylation (RASSF1A, PRSS21, and LINE-1) and N-glycan alterations in blood plasma and seminal plasma samples was investigated using logistic regression models. Pre- and post-radical orchidectomy longitudinal samples from NSE patients were analyzed to assess surgical treatment response and disease monitoring utility.</p><p><strong>Results: </strong>Blood plasma analysis of combined cfDNA and N-glycan profiling demonstrated high diagnostic precision, with an AUC of 0.96, identifying 85% of STM-negative patients and all pure-form teratomas. Post-operative blood plasma analysis showed that LINE-1 cfDNA methylation levels returned to those of healthy controls. Seminal plasma analysis revealed an increased cfDNA fragmentation index (CFI) and cfDNA methylation changes in LINE-1 and PRSS21, with an AUC of 0.83 and identifying 85% of STM-negative patients.</p><p><strong>Conclusion: </strong>The proposed multi-analyte approach significantly improves early diagnostics of NSE, particularly for STM-negative cases and teratomas. LINE-1 cfDNA methylation is a promising biomarker for NSE detection and treatment monitoring. These findings could transform diagnostic strategies and patient management in testicular germ cell tumors, with potential applications in reducing overtreatment and improving outcomes .</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"257"},"PeriodicalIF":5.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12247211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616319","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":"Specificity protein 1 initiates epithelial-mesenchymal transition of circulating tumor cells to inhibit metastasis in prostate cancer.","authors":"Mei Yang, Lin Jie Li, Guo Ping Qiu, Hui Liu, Fei Gao","doi":"10.1186/s12935-025-03888-7","DOIUrl":"10.1186/s12935-025-03888-7","url":null,"abstract":"<p><p>Circulating tumor cells (CTCs), as seeds for metastasis, hold great promise for cancer diagnosis, prognosis, and treatment. Based on the expression of biomarkers, CTCs can be categorized as epithelial (E), mesenchymal (M), or hybrid (M/E) phenotypes. At present, the role of CTC phenotypes in metastatic prostate cancer (PCa) is not clear. In the current study, CTCs were isolated from 102 PCa patients using the Canpatrol™ technology. Fluorescence in situ hybridization (FISH) was used to categorize CTCs. The EMT regulators were analyzed by bioinformatics software. Specificity protein 1 (SP1) was overexpressed in PC3 cells by lentiviral transfection. Transwell assay was used to assess cell invasion in vitro. A mouse model of metastasis was used to evaluate the seeding capability of SP1-overexpressing PC3 cells administered via tail vein injection. It was found that the cell counts of total CTCs (T-CTCs), E-CTCs, and hybrid-CTCs were significantly higher in metastatic PCa than local PCa. T-CTC count (> 14) was identified as an independent risk factor for metastasis, predicting metastatic PCa with a sensitivity of 90.48% and a specificity of 96.67%. SP1 was identified as a valuable EMT regulator by bioinformatics. SP1 overexpression in PC3 cells induced EMT and enhanced cell invasion in vitro, however, it inhibited lung metastasis in vivo. In conclusion, the T-CTC count predicted metastatic PCa. Polarization of PCa CTCs toward the M phenotype reduced their metastasis-initiating capability. SP1 overexpression induced EMT and repressed metastatic colonization of PCa CTCs. Thus, the induction of EMT in CTCs by SP1 augmentation may hold promise as a novel treatment for PCa by staving off metastasis.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"255"},"PeriodicalIF":5.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12247201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616323","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 role of platelets in tumor immune evasion and metastasis: mechanisms and therapeutic implications.","authors":"Jiaqi Gan, Xinjun Zhang, Jie Guo","doi":"10.1186/s12935-025-03877-w","DOIUrl":"10.1186/s12935-025-03877-w","url":null,"abstract":"<p><p>Only circulating tumor cells (CTCs) that successfully evade immune surveillance upon entering the bloodstream can lead to clonal expansion and metastasis. Cancer progression is accompanied by pathophysiological processes such as platelet activation and thrombosis. Platelets secrete a variety of growth factors to stimulate cancer cell proliferation, regulate tumor angiogenesis, and subsequently mediate surface changes in cancer cells to promote invasion and progression. As part of a dangerous alliance, CTCs and platelets induce mutual activation. Activated platelets aggregate and encapsulate tumor cells, forming microtumor thrombi containing fibrin clots that act as protective barriers. These platelets interact with immune cells, including NK cells, macrophages, neutrophils, and T cells, to facilitate cancer metastasis and progression through various mechanisms. The formation of a favorable tumor microenvironment (TME) and pre-metastatic niche aids cancer cells in evading immune surveillance. Multiple signaling pathways and immune checkpoints are also involved in this process. Given the significant role of platelets in tumor immune evasion, anti-cancer strategies targeting platelets and their potential use as \"bionic drug delivery systems\" for anti-tumor drugs hold broad prospects in emerging tumor therapies.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"258"},"PeriodicalIF":5.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12255057/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616325","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":"MicroRNA-1303 in cancer pathogenesis and therapy: clinical implications for biomarker development and targeted treatment strategies.","authors":"Lingzi Zheng, Ling Hu, Bita Badehnoosh","doi":"10.1186/s12935-025-03895-8","DOIUrl":"10.1186/s12935-025-03895-8","url":null,"abstract":"<p><p>Cancer remains one of the most formidable global health challenges due to its complex pathogenesis, late-stage diagnosis, and limited therapeutic options for many subtypes. Despite advancements in reducing cancer-related mortality through lifestyle modifications and early interventions, it continues to rank among the top ten causes of death worldwide. A growing body of evidence highlights the critical role of non-coding RNAs, particularly microRNAs (miRNAs), in cancer biology. MiRNAs are short, non-coding RNA molecules approximately 19-25 nucleotides in length that regulate gene expression at the post-transcriptional level. Among these, miRNA-1303 has garnered increasing attention due to its aberrant expression across a variety of malignancies and its involvement in diverse cellular processes, including cell proliferation, apoptosis, migration, invasion, and chemoresistance. In this review, we provide a comprehensive overview of miRNA-1303, emphasizing its dysregulation in different cancer types such as colorectal, breast, prostate, and lung cancers. We explore the molecular mechanisms and signaling pathways modulated by miRNA-1303, including its interaction with oncogenes, tumor suppressors, and key cellular networks like PI3K/AKT, Wnt/β-catenin, and MAPK pathways. We also discuss its functional role in tumor development and progression, supported by both in vitro and in vivo studies. Furthermore, we evaluate the potential of miRNA-1303 as a clinically relevant biomarker for early cancer detection, prognosis prediction, and treatment monitoring. Its expression patterns have been correlated with tumor stage, metastasis, and patient survival, suggesting promising utility in clinical decision-making. In addition, we explore the emerging therapeutic strategies targeting miRNA-1303, including miRNA mimics, inhibitors, and delivery systems designed to modulate its expression in cancer cells. By synthesizing current findings, this review underscores the clinical significance of miRNA-1303 in oncology and proposes future directions for its application in personalized medicine.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"256"},"PeriodicalIF":5.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12247361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616322","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}