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[微小RNA-155对人肺癌细胞系95D体外生长的影响]

[Effects of microRNA-155 on the growth of human lung cancer cell line 95D 
in vitro].

作者信息

Qin Andong, Zhou Ya, Sheng Meixia, Fei Guangru, Ren Tao, Xu Lin

机构信息

Department of Immunology, Zunyi Medical College, Zunyi 563003, China.

出版信息

Zhongguo Fei Ai Za Zhi. 2011 Jul;14(7):575-80. doi: 10.3779/j.issn.1009-3419.2011.07.03.

DOI:10.3779/j.issn.1009-3419.2011.07.03
PMID:21762626
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6000274/
Abstract

BACKGROUND AND OBJECTIVE

Recent studies suggest that miR-155 is involved in lung tumorgenesis, whereas the precise mechanism has not yet been characterized. The aim of this study is to investigate the effects of over-expression of miR-155 on the growth of human lung cancer 95D cells in vitro and its possible mechanism, and thus to provide experimental evidence for further researching on the role of miR-155 in the pathogenesis and development of lung cancer.

METHODS

miR-155 mimics control and miR-155 mimics were tranfected into human lung cancer 95D cells by FuGENE®HD Transfection Reagent respectively in vitro. The relative expression level of miR-155 in 95D cells was determined using specific probe of real-time PCR after transfection. The proliferation of 95D cells was detected by MTT assay. The cell cycle was analyzed by flow cytometry. The expression of SOS1 protein was measured by Western blot.

RESULTS

Compared with control groups, the expression level of miR-155 was significantly increased in miR-155 mimics transfected group (P<0.05). The proliferation of miR-155-transfected 95D cells was significantly inhibited (P<0.05). The percentage of G0/G1 phase cells was increased significantly in miR-155-transfected 95D cells, while the percentage of S phase was remarkably reduced (P<0.05). Furthermore, the expression of SOS1 in miR-155-transfected 95D cells was significantly down-regulated (P<0.05).

CONCLUSIONS

miR-155 could significantly inhibit the growth of human lung cancer 95D cells in vitro, which might be closely related to miR-155 induced G0/G1 phase arrest.

摘要

背景与目的

近期研究表明miR-155参与肺癌发生，但确切机制尚未明确。本研究旨在探讨miR-155过表达对人肺癌95D细胞体外生长的影响及其可能机制，为进一步研究miR-155在肺癌发病机制及发展中的作用提供实验依据。

方法

体外分别用FuGENE®HD转染试剂将miR-155模拟物对照和miR-155模拟物转染到人肺癌95D细胞中。转染后用实时PCR特异性探针测定95D细胞中miR-155的相对表达水平。用MTT法检测95D细胞的增殖情况。用流式细胞术分析细胞周期。用蛋白质印迹法检测SOS1蛋白的表达。

结果

与对照组相比，miR-155模拟物转染组中miR-155的表达水平显著升高（P<0.05）。miR-155转染的95D细胞增殖受到显著抑制（P<0.05）。miR-155转染的95D细胞中G0/G1期细胞百分比显著增加，而S期百分比显著降低（P<0.05）。此外，miR-155转染的95D细胞中SOS1的表达显著下调（P<0.05）。

结论

miR-155可显著抑制人肺癌95D细胞的体外生长，这可能与miR-155诱导的G0/G1期阻滞密切相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d3/6000274/49264ec2610f/zgfazz-14-7-575-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d3/6000274/6f3b70148b68/zgfazz-14-7-575-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d3/6000274/72268b360763/zgfazz-14-7-575-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d3/6000274/ef0e44f4bdff/zgfazz-14-7-575-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d3/6000274/49264ec2610f/zgfazz-14-7-575-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d3/6000274/6f3b70148b68/zgfazz-14-7-575-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d3/6000274/72268b360763/zgfazz-14-7-575-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d3/6000274/ef0e44f4bdff/zgfazz-14-7-575-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/73d3/6000274/49264ec2610f/zgfazz-14-7-575-4.jpg

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