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miR-21对人胃腺癌细胞增殖和凋亡的影响。

Effects of miR-21 on proliferation and apoptosis in human gastric adenocarcinoma cells.

作者信息

Gu Jun-Bao, Bao Xue-Bin, Ma Zhao

机构信息

Department of Gastrointestinal Surgery, Henan Provincial People's Hospital, Zhengzhou, Henan 450003, P.R. China.

出版信息

Oncol Lett. 2018 Jan;15(1):618-622. doi: 10.3892/ol.2017.6171. Epub 2017 May 15.

DOI:10.3892/ol.2017.6171
PMID:29403555
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5780787/
Abstract

The present study investigated the expression of miR-21 in MGC803 gastric cancer cells and its effects on Bcl-2 expression and cell proliferation, apoptosis, and invasion. In total 50 patients were recruited with gastric cancer who were admitted to the Henan Province People's Hospital. The samples of gastric cancer and the adjacent normal tissues were collected after surgery. We found that mRNA levels of and were significantly elevated in tumor tissues compared to control tissue. The expression of Bcl-2 protein was also elevated in cancerous tissue. This high expression of Bcl-2 was associated with clinical stage, lymph node metastasis, and tumor differentiation degree. Inhibition of miR-21 reduced the levels of and in MGC803 cells, and lowered cell proliferation and invasiveness. These results indicate that miR-21 and Bcl-2 may participate in the occurrence and development of gastric adenocarcinoma, suggesting their potential role as biomarkers and therapeutic targets.

摘要

本研究调查了miR-21在MGC803胃癌细胞中的表达及其对Bcl-2表达、细胞增殖、凋亡和侵袭的影响。共招募了50例入住河南省人民医院的胃癌患者。术后采集胃癌及癌旁正常组织样本。我们发现,与对照组织相比,肿瘤组织中[具体基因1]和[具体基因2]的mRNA水平显著升高。癌组织中Bcl-2蛋白的表达也升高。Bcl-2的这种高表达与临床分期、淋巴结转移和肿瘤分化程度相关。抑制miR-21可降低MGC803细胞中[具体基因1]和[具体基因2]的水平,并降低细胞增殖和侵袭能力。这些结果表明,miR-21和Bcl-2可能参与胃腺癌的发生和发展,提示它们作为生物标志物和治疗靶点的潜在作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dde/5780787/3ad9049ccd19/ol-15-01-0618-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dde/5780787/cbd0f5a480e8/ol-15-01-0618-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dde/5780787/9e3422c16f3b/ol-15-01-0618-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dde/5780787/6daa1265fac6/ol-15-01-0618-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dde/5780787/f21afcc35db8/ol-15-01-0618-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dde/5780787/3ad9049ccd19/ol-15-01-0618-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dde/5780787/cbd0f5a480e8/ol-15-01-0618-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dde/5780787/9e3422c16f3b/ol-15-01-0618-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dde/5780787/6daa1265fac6/ol-15-01-0618-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dde/5780787/f21afcc35db8/ol-15-01-0618-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6dde/5780787/3ad9049ccd19/ol-15-01-0618-g04.jpg

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