Experimental cell research最新文献

{"title":"Phospholipase C δ1 affects integrin-mediated cell adhesion and migration by altering available phosphatidylinositol 4,5-bisphosphate levels","authors":"Atsuko Yoneda ,&nbsp;Ryosuke Fujinaka ,&nbsp;Natsuki Tsuchiya ,&nbsp;Saori Yaita ,&nbsp;Sachi Suzuki ,&nbsp;Yuu Kishi ,&nbsp;Yoshikazu Nakamura ,&nbsp;Reiko Satow ,&nbsp;Kiyoko Fukami","doi":"10.1016/j.yexcr.2025.114857","DOIUrl":"10.1016/j.yexcr.2025.114857","url":null,"abstract":"<div><div>Integrins are primary extracellular matrix receptors that play essential roles in homeostasis and development. Integrin activity is tightly regulated and is associated with conformational states. Although phosphatidylinositol 4,5-bisphosphate (PIP₂), produced by phosphatidylinositol 4-phosphate 5-kinases, is involved in integrin activation, it is unclear whether PIP₂-reducing enzymes affect integrin conformation and integrin-mediated cell behavior by altering PIP₂ levels. Herein, we showed that phospholipase C (PLC) δ1, a PIP₂-hydrolyzing enzyme, affected integrin-mediated cell adhesion and migration. In PLCδ1 null murine fibroblasts and PLCδ1 knockdown-human melanoma cells, integrin-mediated cell behavior and basal PIP₂ levels in the plasma membrane increased compared with those in control cells. PLCδ1 reduction led to increases in the extended conformation of integrin β1 ectodomain and the interaction between integrin and its activator/stabilizer talin in the absence of ligands. Overexpression of full-length-PLCδ1 or its pleckstrin homology domain but not their PIP₂-binding incompetent mutants inhibited the integrin-mediated cell behavior. To understand how altering plasma membrane PIP₂ levels affects integrin-mediated cell behavior, the catalytic domain of PIP₂ phosphatase was used. It reduced the basal levels of plasma membrane PIP₂, inhibited integrin-mediated cell migration, increased the closed conformation of the integrin β1 headpiece, and decreased integrin-talin interaction. These data suggested that the effects of PLCδ1 reduction were due to a PIP₂ increase and that the plasma membrane PIP₂ levels affected integrin conformation in the absence of ligands. Our results revealed that PLCδ1 finely tunes integrin-mediated cell adhesion and migration and integrin conformation by altering available PIP₂ levels in the plasma membrane.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"455 1","pages":"Article 114857"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145755584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic adaptation in colorectal cancer microenvironment: Focus on cancer-associated fibroblasts (CAFs) and tumor-associated macrophages (TAMs)","authors":"Chou-Yi Hsu ,&nbsp;Amr Ali Mohamed Abdelgawwad El-Sehrawy ,&nbsp;Mirza R. Baig ,&nbsp;Zahraa Khudhair ,&nbsp;Saidmurodkhon Murtazaev ,&nbsp;Pareshkumar N. Patel ,&nbsp;Subbulakshmi Ganesan ,&nbsp;Vimal Arora ,&nbsp;Sandeep Kumar Shukla ,&nbsp;Priya Priyadarshini Nayak","doi":"10.1016/j.yexcr.2025.114867","DOIUrl":"10.1016/j.yexcr.2025.114867","url":null,"abstract":"<div><div>Metabolic reprogramming within the tumor microenvironment (TME) is a critical driver of colorectal cancer (CRC) progression, influencing tumor growth, immune evasion, and metastatic dissemination. Cancer-associated fibroblasts (CAFs) undergo adaptive shifts toward aerobic glycolysis, a process often termed the “reverse Warburg effect,” producing high levels of lactate and pyruvate that are shuttled to adjacent CRC cells to fuel oxidative phosphorylation and anabolic biosynthesis. CAFs additionally secrete cytokines and growth factors, including TGF-β, IL-6, and VEGF, which integrate metabolic and signaling networks to stimulate epithelial–mesenchymal transition (EMT), angiogenesis, and metastatic potential. Similarly, tumor-associated macrophages (TAMs) exhibit remarkable metabolic plasticity that correlates with their functional heterogeneity. Beyond the classical M1/M2 dichotomy, TAM subsets display differential reliance on oxidative phosphorylation, fatty acid oxidation, or glycolysis depending on local oxygen and nutrient availability. M2-like TAMs, for example, preferentially use oxidative phosphorylation and fatty acid metabolism to sustain survival in hypoxic niches while secreting immunosuppressive metabolites such as arginase, polyamines, and lactate, which inhibit cytotoxic T-cell function. Crosstalk between CAFs and TAMs amplifies these metabolic adaptations: CAF-derived lactate promotes M2 polarization, while TAMs enhance glycolysis and biosynthetic activity in tumor cells. This study aims to systematically investigate the metabolic reprogramming of CAFs and TAMs within the CRC tumor microenvironment. Specifically, we seek to characterize the metabolic adaptations and heterogeneity of these stromal populations, elucidate their reciprocal interactions with tumor cells, and identify potential metabolic vulnerabilities that can be therapeutically targeted to disrupt tumor growth, immune evasion, and metastatic progression.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"455 1","pages":"Article 114867"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145773883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanistic insights into hypoxia-induced TCF7L2 upregulation and its oncogenic effects on colorectal cancer","authors":"Kang Tang ,&nbsp;Yong Cheng ,&nbsp;Jianping Gong ,&nbsp;Yang Li","doi":"10.1016/j.yexcr.2025.114868","DOIUrl":"10.1016/j.yexcr.2025.114868","url":null,"abstract":"<div><div>Hypoxia plays a crucial role in the advancement of colorectal cancer (CRC); however, the downstream mechanisms facilitated by hypoxia-inducible factor 1α (HIF-1α) remain incompletely understood. This study employed <em>in vitro</em> and <em>in vivo</em> models to investigate the role of transcription factor 7-like 2 (TCF7L2) under hypoxic conditions in CRC. Utilizing reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis, we observed an upregulation of TCF7L2 mRNA and protein expression in Caco-2 and HCT-116 CRC cell lines under hypoxia. Functional assays, including CCK-8, colony and sphere formation, Transwell, flow cytometry, and xenograft tumor models, provided evidence that the knockdown of TCF7L2 leads to the suppression of CRC cell proliferation, the induction of apoptosis, cell cycle arrest at the G0/G1 phase, and a decrease in migration and invasion capabilities. Furthermore, it inhibited epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) characteristics <em>in vitro</em>, while also reducing tumor growth <em>in vivo</em>. Mechanistically, chromatin immunoprecipitation (ChIP) and co-immunoprecipitation (co-IP) assays have elucidated that the expression of TCF7L2 induced by hypoxia is dependent on HIF-1α, which directly binds to hypoxia response elements (HREs) within the TCF7L2 promoter. Additionally, Western blot and experiments employing the PI3K inhibitor LY294002 have demonstrated that TCF7L2 activates the PI3K/AKT signaling pathway, thereby facilitating the proliferation of CRC cells. A clinical analysis of 104 CRC specimens, utilizing immunohistochemistry (IHC) and RT-qPCR, revealed that elevated expression levels of TCF7L2 were significantly associated with advanced T stage, metastasis, and unfavorable prognosis. Spearman correlation analysis confirmed a positive relationship between the expressions of TCF7L2 and HIF-1α, while Kaplan-Meier survival analysis demonstrated that their co-expression was predictive of reduced overall survival. Collectively, these findings position TCF7L2 as a critical downstream effector of HIF-1α in hypoxic CRC, and its mechanistic role in promoting malignancy and correlation with poor prognosis provide a theoretical basis for exploring TCF7L2 as a potential therapeutic target in future studies.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"455 1","pages":"Article 114868"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145789485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"IL-33/ST2 signaling promotes intrahepatic cholangiocarcinoma through reprogramming macrophage polarization via MAPK pathway","authors":"Aimaiti Yasen ,&nbsp;Yichen Tang ,&nbsp;Xiaomin Yang ,&nbsp;Guohua Zuo ,&nbsp;Jun Feng ,&nbsp;Guoying Wang ,&nbsp;Lu Zheng","doi":"10.1016/j.yexcr.2025.114845","DOIUrl":"10.1016/j.yexcr.2025.114845","url":null,"abstract":"<div><h3>Background</h3><div>The role of IL-33/ST2 signaling in reprogramming macrophage polarization within the intrahepatic cholangiocarcinoma (ICC) microenvironment remains poorly understood. This study aimed to elucidate the mechanisms by which IL-33/ST2 signaling regulates macrophage polarization and its impact on ICC progression.</div></div><div><h3>Methods</h3><div>we overexpressed IL-33 in mouse macrophage J774A.1 cells and blocked IL-33/ST2 signaling using a ST2-neutralizing antibody. These macrophages were co-cultured with human ICC cells (HuCCT1 and RBE). Subcutaneous and orthotopic xenograft mouse models of ICC were established to assess the effects of ST2 blockade and adoptive transfer of differentially treated macrophages.</div></div><div><h3>Results</h3><div>IL-33 overexpression in J774A.1 cells significantly increased M2 macrophage marker expression, which was reversed by ST2 neutralization. This was associated with enhanced phosphorylation of ERK1, JNK, and P38, indicating MAPK pathway activation. Co-culture with IL-33-overexpressing macrophages promoted the invasion, migration and epithelial-mesenchymal transition (EMT) of ICC cells, effects that were attenuated by ST2 blockade. In vivo, ST2-neutralizing antibody inhibited ICC tumor growth, while infusion of M2 macrophages promoted it. Xenograft tumor tissues showed elevated expression of IL-33, ST2, M2 markers, and phosphorylated MAPK proteins, which were reduced upon ST2 neutralization.</div></div><div><h3>Conclusion</h3><div>IL-33/ST2 signaling drives ICC progression by promoting M2 macrophage polarization via the MAPK pathway. Targeting this axis may represent a novel therapeutic strategy for ICC.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"455 1","pages":"Article 114845"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145676819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracellular vesicles from tumor-associated macrophages: Implications for tumor progression and emerging therapeutic strategies","authors":"Carolinne Souza Amorim ,&nbsp;João Alfredo Moraes ,&nbsp;Mariana Renovato-Martins ,&nbsp;Juliana Maria Motta","doi":"10.1016/j.yexcr.2025.114855","DOIUrl":"10.1016/j.yexcr.2025.114855","url":null,"abstract":"<div><div>Extracellular vesicles (EVs) derived from tumor cells have been extensively explored over the past decades, as they represent a powerful means of communication that promotes tumor progression, including the formation of pre-metastatic niches and the consequent facilitation of successful metastatic dissemination. However, macrophages comprise a substantial population of non-tumoral cells within the tumor microenvironment and can either facilitate or inhibit tumor progression through the messages carried by their EVs. In this paper, we reviewed the literature on macrophage-derived EVs and their role in modulating tumor behavior, including development, metastasis, immune evasion, and chemoresistance. We begin by outlining the main categories of EVs and the subtypes of macrophage polarization, followed by a discussion of key aspects of macrophage-derived EVs across various tumor types. Finally, we examine emerging therapeutic strategies that utilize these EVs as potential tools in anticancer therapy.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"455 1","pages":"Article 114855"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145751844","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting the Gas6-TAM-SOCS1/3 axis: CP-25 attenuates macrophage dysfunction in primary Sjögren's syndrome","authors":"Yun Chen ,&nbsp;Qianwen Tian ,&nbsp;Meng Yang ,&nbsp;Yunxin Zhang ,&nbsp;Fuxue Kuang ,&nbsp;Lejie Sun ,&nbsp;Qi Xi ,&nbsp;Wendong Xu ,&nbsp;Hongfei Cai ,&nbsp;Yukang Mao ,&nbsp;Tao Wang ,&nbsp;Wei Wei ,&nbsp;Huaxun Wu","doi":"10.1016/j.yexcr.2025.114871","DOIUrl":"10.1016/j.yexcr.2025.114871","url":null,"abstract":"<div><div>The etiology of primary Sjögren's syndrome (pSS) remains largely unexplained to date, and there is a relative lack of effective clinical treatment options.This study aimed to explore the potential therapeutic mechanism of paeoniflorin-6′-O-benzenesulfonate (CP-25) for pSS, especially regarding whether it exerts its effect by regulating the Gas6/TAM signaling axis. The study assessed the expression of the Gas6/TAM axis and its association with macrophage polarization using labial gland tissues, peripheral blood samples from patients with primary Sjögren's syndrome (pSS), and an experimental Sjögren's syndrome mouse model. In vitro, RAW264.7 cells and submandibular gland epithelial cells were employed to analyze changes in the TAM-SOCS1/3 axis, JAK1-STAT1 pathway, and polarization markers (iNOS, Arg1). ELISA was used to detect Gas6 secretion by SGECs, while flow cytometry and confocal microscopy evaluated macrophage function.Both primary Sjögren's syndrome patients and experimental Sjögren's syndrome mice showed dysregulation of the Gas6/TAM signaling pathway, which was closely linked to macrophage polarization imbalance.CP-25 alleviated ESS mouse symptoms by activating the TAM-SOCS1/3 axis, inhibiting the JAK1-STAT1 pathway, and promoting M2 macrophage polarization. In vitro experiments confirmed that CP-25 stimulated salivary gland epithelial cells (SGECs) to secrete Gas6 and reduced matrix metalloproteinase-9 (MMP-9) expression. Moreover, exogenous Gas6 promoted M2 polarization via TAM receptor activation; knockdown of the Mer receptor impaired macrophage phagocytic function. The study also indicated that MMP-9 may be involved in regulating TAM receptors on macrophages.In conclusion, CP-25 treats pSS by regulating SGEC Gas6/MMP-9 secretion, targeting macrophage TAM-SOCS1/3, modulating JAK1-STAT1, and restoring macrophage function.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"455 1","pages":"Article 114871"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145833310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Navigating the nexus: Dysregulation of non-coding RNAs in breast cancer under therapeutic interventions – Mechanisms and clinical implications","authors":"Parisa Alirezae ,&nbsp;Seyed Hossein Khoshraftar ,&nbsp;Saba Hadi ,&nbsp;Akbar Amirfiroozi ,&nbsp;Mohammad M. Pourseif ,&nbsp;Sima Mansoori-Derakhshan","doi":"10.1016/j.yexcr.2025.114854","DOIUrl":"10.1016/j.yexcr.2025.114854","url":null,"abstract":"<div><div>Non-coding RNAs (ncRNAs)—including micro RNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs)—are key regulators of gene expression in the biological processes of breast cancer (BC) development. The dysregulation of these ncRNAs also contributes majorly to the initiation, progression, and treatment resistance of BC. This review summarizes the current understanding of how systemic therapeutic strategies (e.g. chemotherapy, endocrine therapy, targeted therapy, radiotherapy, and immunotherapy) can induce ncRNA changes which subsequently alter treatment responses. The underlying dysregulation of ncRNAs in BC occur through genetic events, epigenetic alterations, and complex transcriptional and post-transcriptional regulatory events, including competing endogenous RNA (ceRNA) networks. Some ncRNAs are important mediators of drug resistance (e.g. miR-21 in chemoresistance, HOTAIR in endocrine resistance, and ncRNAs regulated by ALKBH5 in HER2-targeted therapy resistance), modulating biological pathways such as apoptosis, DNA repair, and drug metabolism. The sensitivity of ncRNAs in biofluids make them appealing candidates for non-invasive biomarkers for diagnosis, prognosis, and real-time monitoring of response to treatment interventions. Despite the clear potential for ncRNAs to serve as therapeutic targets and as biomarkers in clinical management of BC, additional work is required to generate optimal delivery methods, achieve specificity, and standardize detection methods. Future studies, encompassing ‚multi-omics' strategies in BC research together with enhanced computational tools, will also be warranted to fully establish ncRNA discoveries into personalized BC care, and improved treatment outcomes for patient management through precision nanomedicine and liquid biopsy platforms.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"455 1","pages":"Article 114854"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145741836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Timeless prevents senescence-associated phenotypes and enhances DNA repair to promote esophageal cancer cell growth","authors":"Chiaki Noguchi ,&nbsp;Kalisse I. Horne ,&nbsp;Tylor Brewster ,&nbsp;Alyssa Duffy ,&nbsp;Jeel P. Shah ,&nbsp;Amber Theriault ,&nbsp;Olivia El Naggar ,&nbsp;Soumya Vavilala ,&nbsp;Shivani Sheth ,&nbsp;Eishi Noguchi","doi":"10.1016/j.yexcr.2025.114828","DOIUrl":"10.1016/j.yexcr.2025.114828","url":null,"abstract":"<div><div>Esophageal squamous cell carcinoma (ESCC) is one of the deadliest forms of squamous cell carcinoma, comprising approximately 90 % of all esophageal cancer cases. We previously demonstrated that the Fanconi anemia DNA repair (FA) pathway mitigates replication stress to preserve self-renewal capacity of esophageal cancer cells, highlighting the critical role of minimizing replication stress in esophageal cancer proliferation. In this study, to further explore the role of replication stress in esophageal cancer growth, we investigated the function of Timeless, a key subunit of the replication fork protection complex essential for preventing replication stress. Our findings reveal that Timeless is upregulated in esophageal cancer cells, and its depletion increases sensitivity to DNA-damaging agents, inducing cellular senescence in esophageal keratinocytes. Timeless depletion also elevates the DNA damage response while reducing the expression of DNA repair proteins associated with the FA pathway and homologous recombination. Furthermore, the loss of Timeless impairs colony-forming ability in soft agar and diminishes the self-renewal capacity required to form 3D organoids. These results suggest that Timeless plays a critical role in facilitating DNA repair and esophageal cancer progression and may represent a promising target for developing effective therapeutic strategies to treat esophageal cancers.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"455 1","pages":"Article 114828"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145530490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “m6A-mediated upregulation of miRNA-193a aggravates cardiomyocyte apoptosis and inflammatory response in sepsis-induced cardiomyopathy via the METTL3/ miRNA-193a/BCL2L2 pathway” [Exp Cell Res. 2023 Sep 1; 430(1): 113712]","authors":"Lian Liang ,&nbsp;Siqi Liu ,&nbsp;Qingyu Wu ,&nbsp;Ran Chen ,&nbsp;Shanping Jiang ,&nbsp;Zhengfei Yang","doi":"10.1016/j.yexcr.2025.114856","DOIUrl":"10.1016/j.yexcr.2025.114856","url":null,"abstract":"","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"455 1","pages":"Article 114856"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145827194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Migrasomes in the tumor microenvironment: Functional roles and therapeutic potential","authors":"Xinxin Li ,&nbsp;Jinshan Yang ,&nbsp;Hao Xie ,&nbsp;Jiahao Guo ,&nbsp;Jiazi Cha ,&nbsp;Jiahui Wang ,&nbsp;Chunhua Lin","doi":"10.1016/j.yexcr.2025.114865","DOIUrl":"10.1016/j.yexcr.2025.114865","url":null,"abstract":"<div><div>Migrasomes are large extracellular vesicles (0.5–3 μm in diameter) with a distinctive pomegranate-like structure, formed along retraction fibers during cell migration and released their content through migracytosis. Unlike other extracellular vesicles, migrasomes play unique roles in intercellular communication by transferring proteins, RNAs, and signaling molecules within the tumor microenvironment. This review summarizes recent advances in understanding migrasome biogenesis, composition, and functional roles in cancer progression. We highlight their contributions to tumor angiogenesis, extracellular matrix remodeling, and most notably immune escape, through the regulation of tumor-associated macrophages, T cells, and other immune and stromal cells. Pan-cancer evidence supports a strong correlation between migrasome abundance and immunosuppressive gene signatures, including immune checkpoint expression and tumor immune dysfunction and exclusion (TIDE) scores. We also highlight the promising diagnostic and therapeutic potential of migrasomes as novel biomarkers and targets for cancer therapy. Finally, we discuss current research challenges and outline future directions for advancing migrasome research toward clinical translation.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"455 1","pages":"Article 114865"},"PeriodicalIF":3.5,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145755664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}