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微小RNA-122-3p通过靶向A549细胞中的叉头框O抑制肿瘤细胞增殖并诱导凋亡。

MicroRNA-122-3p inhibits tumor cell proliferation and induces apoptosis by targeting Forkhead box O in A549 cells.

作者信息

Wang Wen, Yang Jinsong, Yu Fenglei, Li Wenjie, Wang Li, Zou Haoyu, Long Xia

机构信息

Department of Cardio-Thoracic Surgery, Hunan Provincial People's Hospital, Changsha, Hunan 410005, P.R. China.

Department of Thoracic Surgery, The Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, P.R. China.

出版信息

Oncol Lett. 2018 Feb;15(2):2695-2699. doi: 10.3892/ol.2017.7577. Epub 2017 Dec 11.

Abstract

The imbalance between cell proliferation and apoptosis was implicated to serve key roles in cancer pathogenesis. The characteristics of microRNAs (miRNAs/miRs) have attracted much attention in research focusing on cancer pathogenesis in recent years. miR-122-3p has been reported to be associated with a number of disease processes and pathogenesis, including lung cancer. The present study aimed to investigate the association of miR-122-3p expression level with cell proliferation and apoptosis in a lung cancer cell line. A549 cells were transfected with miR-122-3p to interrupt the expression of miR-122-3p. Subsequently, MTT and BrdU assay, and western blot were used to analyze the influence of miR-122-3p on lung cancer cell proliferation, cell viability and its underlying mechanism. The present study revealed that, by targeting p27, overexpression of miR-122-3p inhibited cell proliferation in lung cancer. Furthermore, the cell apoptosis analysis suggested that overexpression of miR-122-3p was able to inhibit cell apoptosis by targeting Forkhead box O. These findings suggest that miR-122-3p may be associated with the pathology and progression of lung cancer and be a new therapeutic target for this disease.

摘要

细胞增殖与凋亡之间的失衡被认为在癌症发病机制中起关键作用。近年来,微小RNA(miRNA/miR)的特性在关注癌症发病机制的研究中备受关注。据报道,miR-122-3p与包括肺癌在内的多种疾病过程和发病机制相关。本研究旨在探讨miR-122-3p表达水平与肺癌细胞系中细胞增殖和凋亡的关系。用miR-122-3p转染A549细胞以阻断miR-122-3p的表达。随后,采用MTT和BrdU检测以及蛋白质印迹法分析miR-122-3p对肺癌细胞增殖、细胞活力及其潜在机制的影响。本研究表明,通过靶向p27,miR-122-3p的过表达抑制肺癌细胞增殖。此外,细胞凋亡分析表明,miR-122-3p的过表达能够通过靶向叉头框O抑制细胞凋亡。这些发现表明,miR-122-3p可能与肺癌的病理和进展相关,并且是该疾病的一个新的治疗靶点。

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