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微小RNA-106通过调控p21和E2F5对胃癌细胞增殖的影响

Effects of microRNA-106 on proliferation of gastric cancer cell through regulating p21 and E2F5.

作者信息

Yao Yong-Liang, Wu Xiao-Yang, Wu Jian-Hong, Gu Tao, Chen Ling, Gu Jin-Hua, Liu Yun, Zhang Qing-Hui

机构信息

Kunshan First People's Hospital, Affiliated to Jiangsu University, Kunshan, Jiangsu, China.

出版信息

Asian Pac J Cancer Prev. 2013;14(5):2839-43. doi: 10.7314/apjcp.2013.14.5.2839.

Abstract

OBJECTIVE

To investigate the effects of miR-106b on malignant characteristics of gastric cancer cells, and explore possible mechanisms.

METHODS

Expression of miR-106b, p21 and E2F was determined by real-time PCR. Transfection with miR-106b mimics was conducted, and gastric cancer cells with miR-106b overexpression were obtained. Cells transfected with mimic mutants and those without transfection served as negative and blank controls, respectively. Flow cytometry and transwell assays were adopted to detect the effects of miR-106b overexpression on cell cycle, migration and invasion of gastric cancer cells.

RESULTS

. The expression of miR- 106b in gastric cancer cells was significantly higher than that in normal gastric mucosa cells. Furthermore, the expression level of miR-106b rose according to the degree of malignacy among the three GC cell strains (MKN- 45 > SGC-7901 > MKN-28). Overexpression of miR-106b shortened the G0/G1 phase and accelerated cell cycle progression, while reducing p21 and E2F5, without any significant effects on the capacity for migration and invasion of gastric cancer cells.

CONCLUSIONS

miR-106b may promote cell cycling of gastric cancer cells through regulation of p21 and E2F5 target gene expression.

摘要

目的

探讨miR-106b对胃癌细胞恶性特征的影响,并探索其可能机制。

方法

采用实时PCR检测miR-106b、p21和E2F的表达。进行miR-106b模拟物转染,获得miR-106b过表达的胃癌细胞。分别以转染模拟突变体的细胞和未转染的细胞作为阴性对照和空白对照。采用流式细胞术和Transwell实验检测miR-106b过表达对胃癌细胞周期、迁移和侵袭的影响。

结果

胃癌细胞中miR-106b的表达明显高于正常胃黏膜细胞。此外,在三种胃癌细胞株(MKN-45>SGC-7901>MKN-28)中,miR-106b的表达水平随恶性程度升高而升高。miR-106b过表达缩短了G0/G1期,加速了细胞周期进程,同时降低了p21和E2F5的表达,但对胃癌细胞的迁移和侵袭能力无显著影响。

结论

miR-106b可能通过调控p21和E2F5靶基因表达促进胃癌细胞的细胞周期进程。

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