Chinese Journal of Tissue Engineering Research ›› 2016, Vol. 20 ›› Issue (1): 49-54.doi: 10.3969/j.issn.2095-4344.2016.01.009

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Cryptotanshinone effects on the proliferation and apoptosis of renal carcinoma stem cells

Feng Min, Jia Ming-hua   

  1. Department of Nephrology, Zhengzhou Yihe Hospital, Zhengzhou 450008, Henan Province, China
  • Received:2015-11-08 Online:2016-01-01 Published:2016-01-01
  • About author:Feng Min, Associate chief physician, Department of Nephrology, Zhengzhou Yihe Hospital, Zhengzhou 450008, Henan Province, China

Abstract:

BACKGROUND: Previous studies have found that cryptotanshinone represses multiple tumors, but little is reported on its effect on renal carcinoma.
OBJECTIVE: To explore the effect of cryptotanshinone on the proliferation and apoptosis of the renal carcinoma stem cells.
METHODS: CD133+ renal carcinoma stem cells were separated from OS-RC-2 cells by immunomagnetic bead separation. Effects of 0, 0.2, 1, 5 mg/L cryptotanshinone on the proliferation and apoptosis of CD133+ renal carcinoma stem cells were detected by MTT and flow cytometry, respectively. Expression levels of Ki67, Bcl-2, Caspase-3 and p-Caspase-3 protein were detected by western blot assay.
RESULTS AND CONCLUSION: After magnetic cell sorting, the percentage of CD133+ cells was increased from 6.32% to 82.73%, and there was a significant difference before and after cell sorting (P < 0.001). Cryptotanshinone could repress the proliferation of CD133+ renal carcinoma stem cells and promote cell apoptosis in a dose-dependent manner. The protein expression levels of Ki67 and Bcl-2 in the 5 mg/L cryptotanshinone group were significantly decreased compared with the control group, while the protein expression level of p-Caspase-3 protein was significantly increased. In addition, there was no difference in the protein expression of Caspase-3 between cryptotanshinone and control group. These findings indicate that cryptotanshinone may be a potent anticancer drug for the treatment of renal carcinoma by inhibiting expression of Ki67 and Bcl-2 and promoting protein expression of p-Caspase-3. 
 

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