{"title":"LRP11-AS1通过miR-149-3p/CDK4途径介导肠毒性脆弱拟杆菌相关的结直肠癌致癌作用","authors":"Zhongguang Wu, Mengqiu Yu, Yu Zeng, Yingfeng Huang, Weidong Zheng","doi":"10.1038/s41417-024-00862-9","DOIUrl":null,"url":null,"abstract":"<p><p>Long noncoding RNAs (lncRNAs) are critical in tumorigenesis and show potential for tumor diagnosis and therapy. Enterotoxigenic Bacteroides fragilis (ETBF), known for producing enterotoxins, is implicated in human gut tumorigenesis, yet the underlying mechanisms are not fully elucidated. This study aims to clarify the molecular mechanisms by which lncRNAs contribute to ETBF-induced tumorigenesis, with a focus on LRP11-AS1's role in modulating ETBF's colorectal carcinogenesis. We found a marked increase in LRP11-AS1 expression in colorectal cancer (CRC) tissues compared to adjacent non-tumorous tissues. In vitro, CRC cells exposed to ETBF showed elevated LRP11-AS1 levels. Mechanistically, LRP11-AS1 was shown to enhance CDK4 expression by competitively binding to miR-149-3p. These results indicate that LRP11-AS1 may facilitate ETBF-related carcinogenesis in CRC and could serve as a therapeutic target and diagnostic biomarker for ETBF-associated CRC.</p>","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":" ","pages":""},"PeriodicalIF":4.8000,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"LRP11-AS1 mediates enterotoxigenic Bacteroides fragilis-related carcinogenesis in colorectal Cancer via the miR-149-3p/CDK4 pathway.\",\"authors\":\"Zhongguang Wu, Mengqiu Yu, Yu Zeng, Yingfeng Huang, Weidong Zheng\",\"doi\":\"10.1038/s41417-024-00862-9\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Long noncoding RNAs (lncRNAs) are critical in tumorigenesis and show potential for tumor diagnosis and therapy. Enterotoxigenic Bacteroides fragilis (ETBF), known for producing enterotoxins, is implicated in human gut tumorigenesis, yet the underlying mechanisms are not fully elucidated. This study aims to clarify the molecular mechanisms by which lncRNAs contribute to ETBF-induced tumorigenesis, with a focus on LRP11-AS1's role in modulating ETBF's colorectal carcinogenesis. We found a marked increase in LRP11-AS1 expression in colorectal cancer (CRC) tissues compared to adjacent non-tumorous tissues. In vitro, CRC cells exposed to ETBF showed elevated LRP11-AS1 levels. Mechanistically, LRP11-AS1 was shown to enhance CDK4 expression by competitively binding to miR-149-3p. These results indicate that LRP11-AS1 may facilitate ETBF-related carcinogenesis in CRC and could serve as a therapeutic target and diagnostic biomarker for ETBF-associated CRC.</p>\",\"PeriodicalId\":9577,\"journal\":{\"name\":\"Cancer gene therapy\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":4.8000,\"publicationDate\":\"2024-12-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cancer gene therapy\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1038/s41417-024-00862-9\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"BIOTECHNOLOGY & APPLIED MICROBIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer gene therapy","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41417-024-00862-9","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}
LRP11-AS1 mediates enterotoxigenic Bacteroides fragilis-related carcinogenesis in colorectal Cancer via the miR-149-3p/CDK4 pathway.
Long noncoding RNAs (lncRNAs) are critical in tumorigenesis and show potential for tumor diagnosis and therapy. Enterotoxigenic Bacteroides fragilis (ETBF), known for producing enterotoxins, is implicated in human gut tumorigenesis, yet the underlying mechanisms are not fully elucidated. This study aims to clarify the molecular mechanisms by which lncRNAs contribute to ETBF-induced tumorigenesis, with a focus on LRP11-AS1's role in modulating ETBF's colorectal carcinogenesis. We found a marked increase in LRP11-AS1 expression in colorectal cancer (CRC) tissues compared to adjacent non-tumorous tissues. In vitro, CRC cells exposed to ETBF showed elevated LRP11-AS1 levels. Mechanistically, LRP11-AS1 was shown to enhance CDK4 expression by competitively binding to miR-149-3p. These results indicate that LRP11-AS1 may facilitate ETBF-related carcinogenesis in CRC and could serve as a therapeutic target and diagnostic biomarker for ETBF-associated CRC.
期刊介绍：
Cancer Gene Therapy is the essential gene and cellular therapy resource for cancer researchers and clinicians, keeping readers up to date with the latest developments in gene and cellular therapies for cancer. The journal publishes original laboratory and clinical research papers, case reports and review articles. Publication topics include RNAi approaches, drug resistance, hematopoietic progenitor cell gene transfer, cancer stem cells, cellular therapies, homologous recombination, ribozyme technology, antisense technology, tumor immunotherapy and tumor suppressors, translational research, cancer therapy, gene delivery systems (viral and non-viral), anti-gene therapy (antisense, siRNA & ribozymes), apoptosis; mechanisms and therapies, vaccine development, immunology and immunotherapy, DNA synthesis and repair.
Cancer Gene Therapy publishes the results of laboratory investigations, preclinical studies, and clinical trials in the field of gene transfer/gene therapy and cellular therapies as applied to cancer research. Types of articles published include original research articles; case reports; brief communications; review articles in the main fields of drug resistance/sensitivity, gene therapy, cellular therapy, tumor suppressor and anti-oncogene therapy, cytokine/tumor immunotherapy, etc.; industry perspectives; and letters to the editor.
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