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微小RNA-15a抑制CNE1鼻咽癌细胞的增殖并诱导其凋亡。

MicroRNA-15a Inhibits Proliferation and Induces Apoptosis in CNE1 Nasopharyngeal Carcinoma Cells.

作者信息

Zhu Kang, He Ying, Xia Cui, Yan Jing, Hou Jin, Kong Demin, Yang Yeye, Zheng Guoxi

机构信息

Department of Otorhinolaryngology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.

出版信息

Oncol Res. 2016;24(3):145-51. doi: 10.3727/096504016X14611963142290.

DOI:10.3727/096504016X14611963142290
PMID:27458095
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7838691/
Abstract

Nasopharyngeal carcinoma (NPC) is a highly metastatic cancer, frequently occurring in Southeast Asia and Southern China. Several microRNAs (miRNAs) have been shown to have an inhibitive effect on NPC, while the effect of miR-15a on NPC remains unclear. Thus, our study aimed to investigate the potential effect of miR-15a on NPC cell proliferation, apoptosis, and possible functional mechanism. Human NPC CNE1 cells were transfected with miR-15a mimics, miR-15a inhibitors, or a control. Afterward, cell viability and apoptosis were assayed by using CCK-8, BrdU assay, and flow cytometry. Moreover, Western blot was used to detect the expression changes of proliferation and apoptosis of related proteins. As a result, miR-15a overexpression significantly reduced cell proliferation (p < 0.01 or p < 0.001) and induced cell apoptosis (p < 0.001), while miR-15a suppression got the opposite result for cell proliferation and apoptosis. In addition, miR-15a overexpression upregulated the protein levels of p27, GSK-3β, Bax, procaspase 3, and active caspase 3, whereas miR-15a suppression downregulated these proteins. The protein level of p21 was not significantly regulated by miR-15a overexpression or suppression. These results indicated that miR-15a played a role for inhibition of proliferation and induction of apoptosis in CNE1 cells.

摘要

鼻咽癌(NPC)是一种具有高度转移性的癌症,常见于东南亚和中国南方。已有研究表明,几种微小RNA(miRNA)对鼻咽癌具有抑制作用,而miR-15a对鼻咽癌的作用尚不清楚。因此,我们的研究旨在探讨miR-15a对鼻咽癌细胞增殖、凋亡的潜在影响及其可能的作用机制。将miR-15a模拟物、miR-15a抑制剂或对照转染到人鼻咽癌CNE1细胞中。随后,使用CCK-8、BrdU检测法和流式细胞术检测细胞活力和凋亡情况。此外,采用蛋白质印迹法检测相关蛋白增殖和凋亡的表达变化。结果显示,miR-15a过表达显著降低细胞增殖(p<0.01或p<0.001)并诱导细胞凋亡(p<0.001),而抑制miR-15a则对细胞增殖和凋亡产生相反的结果。此外,miR-15a过表达上调了p27、GSK-3β、Bax、procaspase 3和活性caspase 3的蛋白水平,而抑制miR-15a则下调了这些蛋白的水平。miR-15a过表达或抑制对p21蛋白水平无显著调节作用。这些结果表明,miR-15a在CNE1细胞中发挥了抑制增殖和诱导凋亡的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca5c/7838691/820875a17b47/OR-24-145-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca5c/7838691/67cfa46b71f8/OR-24-145-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca5c/7838691/c0e8ee818262/OR-24-145-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca5c/7838691/2db959e53d02/OR-24-145-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca5c/7838691/820875a17b47/OR-24-145-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca5c/7838691/67cfa46b71f8/OR-24-145-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca5c/7838691/c0e8ee818262/OR-24-145-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca5c/7838691/2db959e53d02/OR-24-145-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ca5c/7838691/820875a17b47/OR-24-145-g004.jpg

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