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微小RNA-340抑制子宫内膜癌细胞系RL 95-2中的肿瘤细胞增殖并诱导其凋亡。

MicroRNA-340 Inhibits Tumor Cell Proliferation and Induces Apoptosis in Endometrial Carcinoma Cell Line RL 95-2.

作者信息

Xie Wei, Qin Wen, Kang Yalin, Zhou Ziyan, Qin Aiping

机构信息

Department of Reproductive Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China (mainland).

Department of Pathology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China (mainland).

出版信息

Med Sci Monit. 2016 May 6;22:1540-6. doi: 10.12659/msm.898121.

Abstract

BACKGROUND The purpose of our study was to investigate the functional role of microRNA-340 (miR-340) in endometrial carcinoma (EC). MATERIAL AND METHODS Human EC cell line RL 95-2 was transfected with miR-340 mimics, inhibitors, or controls. After 48 h of transfection, the cell viability was determined by 3-(4, 5-dimethyl-2- thiazolyl)-2, 5-diphenyl -2-H-tetrazolium bromide (MTT) assay. The BrdU assay and apoptosis assay were performed to determine the effects of miR-340 mimics or inhibitors on cell proliferation and apoptosis, respectively. The underlying mechanisms involved in cell proliferation and apoptosis were explored by measuring the protein levels of cell cycle regulators (p27 kinase inhibition protein (KIP) 1 and p21) and apoptosis-related factors (B-cell lymphoma-2 (Bcl-2), Bax, pro-Caspase 3, and active-Caspase-3). RESULTS Overexpression of miR-340 significantly inhibited the cell viability (P<0.05) and cell proliferation (P<0.01) of RL 95-2 cells compared with the control group, but increased the apoptosis (P<0.01). However, suppression of miR-340 had opposite results. Moreover, the protein levels of p27 KIP1, Bax, pro-Caspase 3, and active-Caspase-3 were significantly increased by overexpression of miR-340 but were statistically decreased by suppression of miR-340. Contrary results were found in the protein levels of Bcl-2. However, no significant differences were found in p21 expression. CONCLUSIONS MiRNA-340 acts as an anti-oncogene in EC cell line RL 95-2 by inhibition of tumor cell proliferation and induction of apoptosis.

摘要

背景 我们研究的目的是探讨微小RNA - 340(miR - 340)在子宫内膜癌(EC)中的功能作用。

材料与方法 用miR - 340模拟物、抑制剂或对照转染人EC细胞系RL 95 - 2。转染48小时后,通过3 -(4,5 - 二甲基 - 2 - 噻唑基)- 2,5 - 二苯基 - 2 - H - 溴化四氮唑(MTT)法测定细胞活力。进行BrdU测定和凋亡测定,分别确定miR - 340模拟物或抑制剂对细胞增殖和凋亡的影响。通过测量细胞周期调节因子(p27激酶抑制蛋白(KIP)1和p21)和凋亡相关因子(B细胞淋巴瘤 - 2(Bcl - 2)、Bax、前半胱天冬酶3和活化半胱天冬酶 - 3)的蛋白质水平,探索细胞增殖和凋亡的潜在机制。

结果 与对照组相比,miR - 340的过表达显著抑制了RL 95 - 2细胞的细胞活力(P<0.05)和细胞增殖(P<0.01),但增加了凋亡(P<0.01)。然而,miR - 340的抑制产生了相反的结果。此外,miR - 340的过表达显著增加了p27 KIP1、Bax、前半胱天冬酶3和活化半胱天冬酶 - 3的蛋白质水平,但miR - 340的抑制使其在统计学上降低。在Bcl - 2的蛋白质水平上发现了相反的结果。然而,p21表达没有显著差异。

结论 MiRNA - 340通过抑制肿瘤细胞增殖和诱导凋亡在EC细胞系RL 95 - 2中作为一种抗癌基因发挥作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b5de/4917329/11fee83304ae/medscimonit-22-1540-g001.jpg

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