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TRIP6 作为 miR-7 的靶标,调节结直肠癌细胞的增殖和转移。

TRIP6, as a target of miR-7, regulates the proliferation and metastasis of colorectal cancer cells.

机构信息

Department of Anorectal Surgery, Jiaxing Second Hospital, Jiaxing, Zhejiang, 314000, PR China; Department of Anorectal Surgery, The First Affiliated Hospital of Zhejiang University, Hangzhou, Zhejiang, 310000, PR China.

Department of Anorectal Surgery, Jiaxing Second Hospital, Jiaxing, Zhejiang, 314000, PR China.

出版信息

Biochem Biophys Res Commun. 2019 Jun 18;514(1):231-238. doi: 10.1016/j.bbrc.2019.04.092. Epub 2019 Apr 24.

DOI:10.1016/j.bbrc.2019.04.092
PMID:31029422
Abstract

This study focuses on the role of miR-7 in colorectal cancer (CRC) cells by targeting thyroid receptor interactor protein 6 (TRIP6). Here, we report that miR-7 expression was down-regulated in colorectal cancer tissues and cell lines due to DNA hypermethylation. miR-7 overexpression significantly inhibits the proliferation and migration of CRC cells in vitro. TRIP6 was found to be a direct target gene of miR-7. The proliferation inhibition of CRC cells mediated by miR-7 could be rescued after TRIP6 overexpression in vitro and in vivo. Moreover, overexpression of TRIP6 reduced miR-7 inhibitor-mediated CRC cell migration and invasion. These findings demonstrate that miR-7 could inhibit the proliferation and migration of CRC cells by targeting TRIP6 and that miR-7 might serve as a good strategy for diagnosing and treating CRC.

摘要

本研究通过靶向甲状腺受体相互作用蛋白 6(TRIP6)探讨 miR-7 在结直肠癌(CRC)细胞中的作用。本研究报告称,由于 DNA 过度甲基化,miR-7 在结直肠肿瘤组织和细胞系中的表达下调。miR-7 的过表达可显著抑制 CRC 细胞的体外增殖和迁移。TRIP6 被发现是 miR-7 的直接靶基因。体外和体内过表达 TRIP6 可挽救 miR-7 介导的 CRC 细胞增殖抑制。此外,过表达 TRIP6 降低了 miR-7 抑制剂介导的 CRC 细胞迁移和侵袭。这些发现表明,miR-7 可通过靶向 TRIP6 抑制 CRC 细胞的增殖和迁移,miR-7 可能成为诊断和治疗 CRC 的良好策略。

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