Trichostatin A inducing apoptosis and cell cycle arrest of bladder cancer cells: The in vitro mechanism
- Author:
Wei QU
1
Author Information
1. Department of Kidney Transplantation
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Bladder neoplasms;
Cell cycle;
Enzyme inhibitors;
Histone deacetylases;
Trichostatin A
- From:
Academic Journal of Second Military Medical University
2010;28(3):272-276
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the influence of trichostatin A (TSA), a histone deacetylase (HDAC) inhibitor, on the growth of human bladder cancer cells and on the expression of related genes, and to explore the mechanism involved. Methods: MTT assay was employed to evaluate the inhibitory effect of TSA (0.05, 0.1, 0.2, 0.4, 0.8 μmol/L) on growth of human T24 bladder cancer cells. The morphological changes of T24 cells were observed by transmission electron microscope after treated with 0.4 μmol/L TSA; the cell cycle distribution and apoptotic ratio were determined by flow cytometry. The acetyl level of histone after TSA treatment was detected by Western blot; the mRNA expression of p21CIP1/WAF1, cyclin A, and cyclin E was measured by FQ-PCR. Results: MTT assay revealed TSA inhibited the growth of T24 cells in a concentration- and time-dependent manner. Typical morphological changes of apoptotic cells were observed by electron microscope after treatment with 0.4 μmol/L TSA. Flow cytometry showed that the cells were blocked at G0/G1 phase and typical Sub-G1 peak appeared. TSA obviously promoted the acetyl level of histone, induced expression of p21CIP1/WAF1 mRNA, and inhibited expression of cyclin A, but had no obvious influence on expression of cyclin E. Conclusion: TSA can inhibit bladder cancer cells through inducing cell apoptosis and cell cycle arrest in vitro, which might be related to the acetyl level of histone and the expression of p21CIP1/WAF1 and cyclin A.
