ScholarLens Back to search
2005•Zhongguo xiandai yixue/Zhongguo xiandai yixue zazhiRequires access

Inhibitory effect of TSA on growth of bladder carcinoma cells and its mechanism

Zhangqun Ye

Open publisher page 0 citations

Abstract

This study was designed to investigate whether trichostatin A (TSA) possesses antitumor activity against Human bladder cancer cell and if any, its mechanism. Human bladder cancer BIU-87 cell lines was treated with different concentrations of TSA for different periods of time. After treatment, cell growth was measured by MTT assay. Cell apoptosis and changes in cell cycle were examined by means of flow cytometry (FCM). p21WAF1 mRNA expression was assessed by RT-PCR. TSA inhibited the proliferation of bladder cancer cell lines significantly at nanomolar concentrations in a time-and dose-dependent fashion, TSA treatment caused cell cycle arrest at G1 phase as shown by FCM and induced p21WAF1 mRNA expression. [Conclusion] TSA is able to inhibit bladder cancer cell lines growth in vitro, most likely through induction of p21WAF1 expression and subsequent arrest of cell cycling at G1 phase.

About this research paper

What this paper is about

This study was designed to investigate whether trichostatin A (TSA) possesses antitumor activity against Human bladder cancer cell and if any, its mechanism. Human bladder cancer BIU-87 cell lines was treated with different concentrations of TSA for different periods of time. After treatment, cell growth was measured by MTT assay. Cell apoptosis and changes in cell cycle were examined by means of flow cytometry (FCM). p21WAF1 mRNA expression was assessed by RT-PCR. TSA inhibited the proliferation of bladder cancer cell lines significantly at nanomolar concentrations in a time-and dose-dependent fashion, TSA treatment caused cell cycle arrest at G1 phase as shown by FCM and induced p21WAF1 mRNA expression. [Conclusion] TSA is able to inhibit bladder cancer cell lines growth in vitro, most likely through induction of p21WAF1 expression and subsequent arrest of cell cycling at G1 phase.

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

This study was designed to investigate whether trichostatin A (TSA) possesses antitumor activity against Human bladder cancer cell and if any, its mechanism. Human bladder cancer BIU-87 cell lines was treated with different concentrations of TSA for different periods of time. After treatment, cell growth was measured by MTT assay. Cell apoptosis and changes in cell cycle were examined by means of flow cytometry (FCM). p21WAF1 mRNA expression was assessed by RT-PCR. TSA inhibited the proliferation of bladder cancer cell lines significantly at nanomolar concentrations in a time-and dose-dependent fashion, TSA treatment caused cell cycle arrest at G1 phase as shown by FCM and induced p21WAF1 mRNA expression. [Conclusion] TSA is able to inhibit bladder cancer cell lines growth in vitro, most likely through induction of p21WAF1 expression and subsequent arrest of cell cycling at G1 phase.

Key concepts: Cell cycle, Flow cytometry, Apoptosis, Cell growth, Bladder cancer, Trichostatin A, Cell culture, Cell cycle checkpoint

Related papers

Related paper 1Related paper 2Related paper 3
Back to paper searchBrowse research topicsOriginal source
Inhibitory effect of TSA on growth of bladder carcinoma cells and its mechanism — Research Paper | ScholarLens