2012•Unpublished venueRequires access

Effect of short hairpin RNA of Bcl-xL gene on biological behaviors of HepG-2 cells

Duan MengxiYuan, HongWang Nan, Li ShijunJiang Yanmei

Open publisher page 0 citations

Abstract

To investigate the inhibitory effect of short hairpin RNA (shRNA) targeting the Bcl-xL gene on the apoptosis and proliferation of hepatocellular carcinoma HepG-2 cells. We constructed Bcl-xL shRNA, and trans- fected it into HepG-2 cells, then detected Bcl-xL gene expression on mRNA and protein levels by reverse tran- scription-polymerase chain reaction (RT-PCR) and flow cytometry, respectively. Cell proliferation was detected by MTT assay. Cell apoptosis and Bcl-2 and Bax expression were detected by flow cytometry. The expression of Bcl-xL was obviously inhibited by RNA interference. The inhibi- tion rates of Bcl-xL mRNA and protein were 86.6 and 70.2%, respectively. Bcl-xL shRNA inhibited cell prolifer- ation (P 0.05), whereas promoted apoptosis (P 0.01). After transfection of Bcl-xL shRNA in HepG-2 cells, the expression of Bcl-2 did not change, but Bax increased sig- nificantly. Bcl-xL shRNA effectively inhibits Bcl-xL gene expression and proliferation of HepG-2 cells and promotes apoptosis.

About this research paper

What this paper is about

To investigate the inhibitory effect of short hairpin RNA (shRNA) targeting the Bcl-xL gene on the apoptosis and proliferation of hepatocellular carcinoma HepG-2 cells. We constructed Bcl-xL shRNA, and trans- fected it into HepG-2 cells, then detected Bcl-xL gene expression on mRNA and protein levels by reverse tran- scription-polymerase chain reaction (RT-PCR) and flow cytometry, respectively. Cell proliferation was detected by MTT assay. Cell apoptosis and Bcl-2 and Bax expression were detected by flow cytometry. The expression of Bcl-xL was obviously inhibited by RNA interference. The inhibi- tion rates of Bcl-xL mRNA and protein were 86.6 and 70.2%, respectively. Bcl-xL shRNA inhibited cell prolifer- ation (P 0.05), whereas promoted apoptosis (P 0.01). After transfection of Bcl-xL shRNA in HepG-2 cells, the expression of Bcl-2 did not change, but Bax increased sig- nificantly. Bcl-xL shRNA effectively inhibits Bcl-xL gene expression and proliferation of HepG-2 cells and promotes apoptosis.

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

To investigate the inhibitory effect of short hairpin RNA (shRNA) targeting the Bcl-xL gene on the apoptosis and proliferation of hepatocellular carcinoma HepG-2 cells. We constructed Bcl-xL shRNA, and trans- fected it into HepG-2 cells, then detected Bcl-xL gene expression on mRNA and protein levels by reverse tran- scription-polymerase chain reaction (RT-PCR) and flow cytometry, respectively. Cell proliferation was detected by MTT assay. Cell apoptosis and Bcl-2 and Bax expression were detected by flow cytometry. The expression of Bcl-xL was obviously inhibited by RNA interference. The inhibi- tion rates of Bcl-xL mRNA and protein were 86.6 and 70.2%, respectively. Bcl-xL shRNA inhibited cell prolifer- ation (P 0.05), whereas promoted apoptosis (P 0.01). After transfection of Bcl-xL shRNA in HepG-2 cells, the expression of Bcl-2 did not change, but Bax increased sig- nificantly. Bcl-xL shRNA effectively inhibits Bcl-xL gene expression and proliferation of HepG-2 cells and promotes apoptosis.

Key concepts: Small hairpin RNA, Bcl-xL, Molecular biology, Apoptosis, Transfection, RNA interference, Flow cytometry, Gene expression

Related papers

Back to paper searchBrowse research topicsOriginal source
Effect of short hairpin RNA of Bcl-xL gene on biological behaviors of HepG-2 cells — Research Paper | ScholarLens