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癌症中的c-Met与微小RNA

c-Met and miRs in Cancer.

作者信息

Giglio Simona, Vecchione Andrea

机构信息

Department of Clinical and Molecular Medicine, Sapienza University of Rome, Rome 00161, Italy.

出版信息

Biomedicines. 2015 Jan 5;3(1):32-44. doi: 10.3390/biomedicines3010032.

DOI:10.3390/biomedicines3010032
PMID:28536397
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5344231/
Abstract

c-Met, a member of the receptor tyrosine kinase family, is involved in a wide range of cellular processes, including tumor survival, cell growth, angiogenesis and metastasis, and resulting in overexpression in many human cancers, leading to a constitutive activation of the downstream pathways. Recently identified MicroRNAs are a family of small noncoding RNA molecules, extensively studied in cancer, that exert their action by inhibiting gene expression at the posttranscriptional level in several biological processes. Aberrant regulation of microRNAs expression has been implicated in the pathogenesis of different human neoplasia. Several publications point out the connections between c-Met and its ligand hepatocyte growth factor (HGF) and microRNAs. This review summarizes the current knowledge about the interplay between c-Met/HGF and microRNAs and provides evidence that microRNAs are a novel and additional system to regulate c-Met expression in tumors. In the future, microRNAs connected to c-Met may provide an additional option to inhibiting this oncogene from orchestrating an invasive growth program.

摘要

c-Met是受体酪氨酸激酶家族的成员之一,参与多种细胞过程,包括肿瘤存活、细胞生长、血管生成和转移,在许多人类癌症中导致过表达,从而导致下游通路的组成性激活。最近发现的微小RNA是一类小的非编码RNA分子,在癌症研究中得到广泛研究,它们通过在几个生物学过程的转录后水平抑制基因表达来发挥作用。微小RNA表达的异常调节与不同人类肿瘤的发病机制有关。一些出版物指出了c-Met及其配体肝细胞生长因子(HGF)与微小RNA之间的联系。本综述总结了目前关于c-Met/HGF与微小RNA相互作用的知识,并提供证据表明微小RNA是调节肿瘤中c-Met表达的一种新的额外系统。未来,与c-Met相关的微小RNA可能为抑制这种癌基因协调侵袭性生长程序提供额外的选择。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89c/5344231/12299f6b0a3a/biomedicines-03-00032-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89c/5344231/1c5ac4f96c09/biomedicines-03-00032-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89c/5344231/12299f6b0a3a/biomedicines-03-00032-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89c/5344231/1c5ac4f96c09/biomedicines-03-00032-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d89c/5344231/12299f6b0a3a/biomedicines-03-00032-g002.jpg

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Biochem Biophys Res Commun. 2014 Aug 8;450(4):1304-12. doi: 10.1016/j.bbrc.2014.06.142. Epub 2014 Jul 21.
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MicroRNA-34a overcomes HGF-mediated gefitinib resistance in EGFR mutant lung cancer cells partly by targeting MET.微小RNA-34a部分通过靶向MET克服了HGF介导的EGFR突变肺癌细胞对吉非替尼的耐药性。
Cancer Lett. 2014 Sep 1;351(2):265-71. doi: 10.1016/j.canlet.2014.06.010. Epub 2014 Jun 28.
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微小RNA在胶质母细胞瘤中调控PI3K/AKT信号通路的作用
Iran J Pathol. 2022 Spring;17(2):122-136. doi: 10.30699/IJP.2022.539029.2726. Epub 2022 Mar 8.
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Dual inhibition of RNAi therapeutic miR-26a-5p targeting cMet and immunotherapy against EGFR in endometrial cancer treatment.在子宫内膜癌治疗中,对靶向cMet的RNAi治疗性miR-26a-5p进行双重抑制以及针对EGFR的免疫治疗。
Ann Transl Med. 2021 Jan;9(1):5. doi: 10.21037/atm-20-3166.
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