辣椒素引發人類膀胱癌

細胞凋亡及細胞生長抑制之探討

林明鴻^1,2、闕斌如²

¹臺南市立安南醫院-委託中國醫藥大學興建經營 外科部 泌尿科；²國立中興大學生命科學院生物醫學研究所

CAPSAICIN INDUCES APOPTOSIS AND CELL CYCLE ARREST IN BLADDER CANCER TSGH-8301 CELLS

Ming-Hung Lin^1,2, Pin-Ju Chueh²

Divisions of Urology, Department of Surgery, China Medical University-An Nan Hospital¹; Institute of Biomedical Sciences, National Chung Hsing University, Taichung, Taiwan, ROC

Purpose: To explore the involvement of tNOX in capsaicin-exposed bladder cancer cells, particularly, apoptotic signaling pathways.

Materials and Methods: In this study, we investigated the effect of capsaicin on human bladder cancer cell lines TSGH 8301, and tried to clarify the relevant inhibition of cancer of the mechanism. The cell numbers were detected by flowcytometry. ROS and MMP assay were used to check cell survival stress and mitochondrial permeability. Western blot analysis was used to study protein expression profiles of apoptosis and cell cycle arrest.

Results: We found that the TSGH 8301 cell growth was inhibited by capsaicin with dose dependent and there was significant cell apoptosis. The cell cycle arrested at G1 / S phase. The ROS assay and MMP assay significantly revealed increased cell survival stress and mitochondrial permeability. By  the Western blot analysis, we found that in 100uM and 200uM concentration of capsaicin, cleaved PARP, P53 expression increased, and Bcl-2, Rb, p-Rb, CDK2 decreased performance indicated that capsaicin induce cell cycle arrest and apoptosis of TSGH 8301 cells. And in 10uM concentration of capsaicin, there was no increase in cancer cell growth, and no inhibition of the growth of the cancer  cells.

      Western blot analysis found that capsaicin inhibited expression of SIRT1 and tNOX, and the expression of its downstream p53 protein acetylation degree was also affected. Capsaicin presumed to influence cell growth of TSGH 8301 cells through tNOX and SIRT1 protein.

Conclusions:

         Capsaicin cause bladder cancer cell lines TSGH8301 growth arrest and apoptosis, possibly through tNOX and SIRT1 regulatory pathways.