[Induction of cell cycle arrest in bladder cancer RT4 cells by capsaicin]

Zhonghua Yi Xue Za Zhi. 2010 May 11;90(18):1230-3.
[Article in Chinese]

Abstract

Objective: To study the effects of capsaicin on the growth of bladder cancer RT4 cell and its potential mechanism.

Methods: Cell counting kit-8 (CCK-8) assay and flow cytometry were employed to observe the effects of capsaicin (50, 100, 150, 200, 250 micromol/L) on cell growth, cell cycle and apoptosis. Capsaicin (0 micromol/L) was used as a control. The effects of mRNA and protein of transient receptor potential cation channel subfamily V 1 (TRPV1) on RT4 cells were tested by RT-PCR and immunofluorescence respectively. And the expressions of cell cycle protein P53, P21, CDK2 were detected by Western blot after the treatment of capsaicin.

Results: 100 micromol/L capsaicin significantly decreased the viability of RT4 cell [82.0% +/- 6.2% vs 100.0% +/- 12.4% (control), P = 0.036] while the cell viability was 7.8% +/- 2.9% at 250 micromol/L (P = 0.000). It was in a dose-dependent manner. On the other hand, capsaicin induced the cell cycle arrest of bladder cancer RT4 cells G(0)/G(1) phase in a dose-dependent way. The cell proportion of G(0)/G(1) phase in the control was 37.4% +/- 5.6%, however, it was 72.4% +/- 5.3% at 250 micromol/L (P = 0.000). It was showed that TRPV1 mRNA and protein were expressed in RT4 cells. After a 48-hour treatment with capsaicin, the expressions of P53 and P21 were up-regulated in contrary to the expression of CDK2.

Conclusion: Capsaicin induces the cell cycle arrest of bladder cancer RT4 cells G(0)/G(1) phase and growth inhibition via TRPV1 receptor by modulating the expression of P53, P21 and CDK2.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects
  • Capsaicin / pharmacology*
  • Cell Cycle / drug effects*
  • Cell Line, Tumor
  • Cell Proliferation / drug effects
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism
  • Humans
  • TRPV Cation Channels / metabolism*
  • Tumor Suppressor Protein p53 / metabolism
  • Urinary Bladder Neoplasms / metabolism*

Substances

  • CDKN1A protein, human
  • Cyclin-Dependent Kinase Inhibitor p21
  • TRPV Cation Channels
  • TRPV1 receptor
  • Tumor Suppressor Protein p53
  • Capsaicin