Abstract Title:

Capsaicin induces cycle arrest by inhibiting cyclin-dependent-kinase in bladder carcinoma cells.

Abstract Source:

Int J Urol. 2012 Jul ;19(7):662-8. Epub 2012 Mar 29. PMID: 22462738

Abstract Author(s):

Dong Chen, Zhonghua Yang, Yongzhi Wang, Guanbin Zhu, Xinghuan Wang

Article Affiliation:

Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.

Abstract:

OBJECTIVE: Capsaicin is a specialized agonist of transient receptor potential vanilloid type 1 Ca2(+) channel, a member of the vanilloid receptor family of cation channels. We aimed to investigate the effects of capsaicin on the proliferation and cell death of human bladder cancer cells.

METHODS: Human bladder cancer cell line 5637 was cultured and the expression of transient receptor potential vanilloid type 1 verified by immunofluorescence and Western blot. Cells were given different disposals (different capsaicin concentration with/without pre-treating with capsazepine; capsazepine, acting as a competitive antagonist of capsaicin) to observe cell viability, cell cycle and cell death by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide assay and flow cytometry. The apoptosis indexes, such as intracellular production of reactive oxygen species and mitochondrial membrane potential were assessed to elucidate the potential mechanism of capsaicin effects in the cells.

RESULTS: Capsaicin decreased the viability of 5637 cells in a dose-dependent way. The flow cytometry outcome showed that capsaicin blocked the cell cycle in the G0/G1 period. The Western blot of cyclin-dependent-kinase involved in G1/S transfer verified this. Meanwhile, increased reactive oxygen species production and decreased mitochondrial membrane potential were detected in capsaicin-treated groups.

CONCLUSIONS: Capsaicin induces cell death through increased reactive oxygen species and decreased mitochondrial membrane potential. Furthermore, capsaicin inhibits the proliferation of 5637 bladder carcinoma cells by cycle arrest with the inhibition of CDK2, CDK4 and CDK6.

Study Type : In Vitro Study

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