Cancer-associated fibroblast-derived exosomal LINC00930 represses cell malignancy and glycolysis by recruiting MBNL1 and elevating PRKAA2 stability in colorectal cancer.
{"title":"Cancer-associated fibroblast-derived exosomal LINC00930 represses cell malignancy and glycolysis by recruiting MBNL1 and elevating PRKAA2 stability in colorectal cancer.","authors":"Chunhui Cui, Lifeng Wang, Jinlong Yu, Changhui Yu, Huiyan Zhang","doi":"10.1186/s40001-026-04022-7","DOIUrl":null,"url":null,"abstract":"<p><p>Exosomes (EXOs) secreted by cancer-associated fibroblasts (CAFs) can induce malignant phenotypes of tumor cells. The long non-coding RNA LINC00930 is known for promoting cancer cell glycolysis and proliferation. However, its role and mechanism in colorectal cancer (CRC) are unclear. This study aimed to determine whether CAF-derived exosomal LINC00930 is involved in CRC progression. In our study, LINC00930 was significantly downregulated in CRC samples and cell lines, as well as in CAFs and CAF-derived EXOs. Functionally, CAF-derived exosomal LINC00930 inhibited CRC cell proliferation, migration, invasion, and glycolysis in vitro and impaired tumor growth in patient-derived xenograft models. LINC00930 improved PRKAA2 stability by recruiting MBNL1. Furthermore, PRKAA2 silencing partly reversed CAF-derived exosomal LINC00930-mediated effects on CRC cell proliferation, migration, invasion, and glycolysis. In conclusion, this study identifies LINC00930 as a tumor-suppressive lncRNA delivered by CAF-derived EXOs that inhibits CRC progression through the MBNL1-PRKAA2 axis, suggesting that LINC00930 could be a viable therapeutic target for CRC.</p>","PeriodicalId":11949,"journal":{"name":"European Journal of Medical Research","volume":" ","pages":""},"PeriodicalIF":4.8000,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"European Journal of Medical Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1186/s40001-026-04022-7","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0
Abstract
Exosomes (EXOs) secreted by cancer-associated fibroblasts (CAFs) can induce malignant phenotypes of tumor cells. The long non-coding RNA LINC00930 is known for promoting cancer cell glycolysis and proliferation. However, its role and mechanism in colorectal cancer (CRC) are unclear. This study aimed to determine whether CAF-derived exosomal LINC00930 is involved in CRC progression. In our study, LINC00930 was significantly downregulated in CRC samples and cell lines, as well as in CAFs and CAF-derived EXOs. Functionally, CAF-derived exosomal LINC00930 inhibited CRC cell proliferation, migration, invasion, and glycolysis in vitro and impaired tumor growth in patient-derived xenograft models. LINC00930 improved PRKAA2 stability by recruiting MBNL1. Furthermore, PRKAA2 silencing partly reversed CAF-derived exosomal LINC00930-mediated effects on CRC cell proliferation, migration, invasion, and glycolysis. In conclusion, this study identifies LINC00930 as a tumor-suppressive lncRNA delivered by CAF-derived EXOs that inhibits CRC progression through the MBNL1-PRKAA2 axis, suggesting that LINC00930 could be a viable therapeutic target for CRC.
期刊介绍:
European Journal of Medical Research publishes translational and clinical research of international interest across all medical disciplines, enabling clinicians and other researchers to learn about developments and innovations within these disciplines and across the boundaries between disciplines. The journal publishes high quality research and reviews and aims to ensure that the results of all well-conducted research are published, regardless of their outcome.