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c-Met调控的癌症中的微小RNA和长链非编码RNA

MicroRNAs and Long Non-coding RNAs in c-Met-Regulated Cancers.

作者信息

Zhan Hong, Tu Sheng, Zhang Feng, Shao Anwen, Lin Jun

机构信息

Women's Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

State Key Laboratory for Diagnosis and Treatment of Infectious Diseases, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.

出版信息

Front Cell Dev Biol. 2020 Mar 11;8:145. doi: 10.3389/fcell.2020.00145. eCollection 2020.

DOI:10.3389/fcell.2020.00145
PMID:32219093
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7078111/
Abstract

MicroRNAs (miRNAs) and long non-coding RNAs (lncRNAs) are components of many signaling pathways associated with tumor aggressiveness and cancer metastasis. Some lncRNAs are classified as competitive endogenous RNAs (ceRNAs) that bind to specific miRNAs to prevent interaction with target mRNAs. Studies have shown that the hepatocyte growth factor/mesenchymal-epithelial transition factor (HGF/c-Met) pathway is involved in physiological and pathological processes such as cell growth, angiogenesis, and embryogenesis. Overexpression of c-Met can lead to sustained activation of downstream signals, resulting in carcinogenesis, metastasis, and resistance to targeted therapies. In this review, we evaluated the effects of anti-oncogenic and oncogenic non-coding RNAs (ncRNAs) on c-Met, and the interactions among lncRNAs, miRNAs, and c-Met in cancer using clinical and tissue chromatin immunoprecipition (ChIP) analysis data. We summarized current knowledge of the mechanisms and effects of the lncRNAs/miR-34a/c-Met axis in various tumor types, and evaluated the potential therapeutic value of lncRNAs and/or miRNAs targeted to c-Met on drug-resistance. Furthermore, we discussed the functions of lncRNAs and miRNAs in c-Met-related carcinogenesis and potential therapeutic strategies.

摘要

微小RNA(miRNA)和长链非编码RNA(lncRNA)是许多与肿瘤侵袭性和癌症转移相关的信号通路的组成部分。一些lncRNA被归类为竞争性内源RNA(ceRNA),它们与特定的miRNA结合,以阻止其与靶mRNA相互作用。研究表明,肝细胞生长因子/间充质-上皮转化因子(HGF/c-Met)通路参与细胞生长、血管生成和胚胎发生等生理和病理过程。c-Met的过表达可导致下游信号的持续激活,从而引发癌变、转移以及对靶向治疗的耐药性。在本综述中,我们利用临床和组织染色质免疫沉淀(ChIP)分析数据,评估了抑癌和致癌非编码RNA(ncRNA)对c-Met的影响,以及lncRNA、miRNA和c-Met在癌症中的相互作用。我们总结了lncRNA/miR-34a/c-Met轴在各种肿瘤类型中的作用机制和影响的现有知识,并评估了靶向c-Met的lncRNA和/或miRNA对耐药性的潜在治疗价值。此外,我们还讨论了lncRNA和miRNA在c-Met相关癌变中的功能以及潜在的治疗策略。

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本文引用的文献

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Lnc-TALC promotes O-methylguanine-DNA methyltransferase expression via regulating the c-Met pathway by competitively binding with miR-20b-3p.Lnc-TALC 通过竞争性结合 miR-20b-3p 调控 c-Met 通路促进 O-甲基鸟嘌呤-DNA 甲基转移酶表达。
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MicroRNA-34a suppresses human lens epithelial cell proliferation and migration via downregulation of c-Met.
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Targeting c-Met in Cancer Therapy: Unravelling Structure-activity Relationships and Docking Insights for Enhanced Anticancer Drug Design.癌症治疗中靶向c-Met:揭示结构-活性关系及对接见解以优化抗癌药物设计
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