Advertisement

 

 

RNAi-mediated TCF-3 gene silencing inhibits proliferation of Eca-109 esophageal cancer cells by inducing apoptosis.

RNAi-mediated TCF-3 gene silencing inhibits proliferation of Eca-109 esophageal cancer cells by inducing apoptosis.
Author Information (click to view)

Ma J, Wang XB, Li R, Xuan SH, Wang F, Li XH, Zhang ZP, Tan L, Li L,


Ma J, Wang XB, Li R, Xuan SH, Wang F, Li XH, Zhang ZP, Tan L, Li L, (click to view)

Ma J, Wang XB, Li R, Xuan SH, Wang F, Li XH, Zhang ZP, Tan L, Li L,

Advertisement
Share on FacebookTweet about this on TwitterShare on LinkedIn

Bioscience reports 2017 11 0937(6) pii 10.1042/BSR20170799

Abstract

Esophageal cancer (EC) remains an important health problem in China. In the present study, through the use of siRNA, specific gene knockdown of transcription factor 3 gene (TCF-3) was achieved in vitro and the effect of TCF-3 gene on human EC Eca-109 cell proliferation and apoptosis. Eca-109 cells were treated using negative control (NC) of siRNA against TCF-3 (siTCF-3) and siTCF-3 group. Colony formation assay was used to detect the colony formation ability in Eca-109 cells. MTT assay was used to measure the cell growth and viability, whereas BrDU assay was used to evaluate cell proliferation, and flow cytometry (FCM) to assess cell apoptosis. Reverse-transcription quantitative PCR (RT-qPCR) was applied to measure TCF-3 gene expression. Protein expressions of TCF-3, apoptosis-related proteins, Bcl-2, Bax, and caspase-3 were determined using Western blotting. Transfection of siTCF-3 successfully down-regulated TCF-3 gene expression. In addition, siTCF-3, reduced Eca-109 cell viability and proliferation, in a time-dependent manner, and inhibited progression of cell cycle from G0/G1 to S-stage. When treated with siTCF-3, the Eca-109 cells exhibited increased apoptosis, with up-regulated cleaved caspase and Bax expressions, whereas Bcl-2 expression was down-regulated. The present study shows that TCF-3 gene silencing inhibits Eca-109 cell growth and proliferation, suppresses cell cycle progression, and promotes apoptosis, which might serve as a new objective for EC treatment.

Submit a Comment

Your email address will not be published. Required fields are marked *

twelve − 10 =

[ HIDE/SHOW ]