Study on apoptosis of the HCT116 cells mediated by cisplatin and its mechanisms
10.3760/cma.j.issn.1008-6315.2009.10.026
- VernacularTitle:顺铂诱导直肠癌HCT116细胞凋亡及其作用机制的研究
- Author:
Yunchun LI
;
Li ZHONG
;
Xiuying TANG
;
Tao MA
- Publication Type:Journal Article
- Keywords:
Rectal carcinoma;
Apoptosis;
Cisplatin
- From:
Clinical Medicine of China
2009;25(10):1076-1079
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the apoptosis mediated by cisplatin on human colorectal tumors (HCT116) cell line and its mechanisms in vitro. Methods The apoptosis levels of HCT116 cells mediated by cisplatin at vari-ous time and in different concentration were measured by M30-ApoptosisTM -ELISA-kits and flow cytometry assay. The expressions of the protein p53,p21 and Bcl-2 were assessed through Western-Blotting. Results Cisplatin in-hibited the proliferation in a time-and dose -dependant manner ( F = 1129. 383, P = 0. 000 and F = 125. 267, P = 0. 000, respectively). The sub-G1 peak detected by flow cytometry at 24,48,72 hours of the apoptosis rates showed a significant difference between the experimental group and the control group (χ2= 5. 669,14.110,12. 221, P = 0. 010,0.003,0. 000,respectively). We found significant differences on the HCT116 cell growth between different time under cisplatin effect (χ2 = 14.008 ,P =0. 003 ). There were significant difference on the CK18-Asp237-Asp396 re-leased by HCT116 cell between different casplatin concentration (F =48. 667 ,P =0.000) as well as different times ( F = 1194. 394, P = 0.000). The Western-Blotting results indicated that the expression level of the p53 ( t = 9.873, -2.906,7. 229,2.776,P =0.000,0. 007,0. 000,0. 011 ) and p21 (t = - 10. 692, - 8. 867, - 15. 063, - 16.281, P = 0. 000,0.001,0.000,0.000 ,respectively) increased gradually, while there are no effect on the expression of the protein Bcl-2(t=1.429,2.011,2.247,2.001,P=0. 178,0.069,0.053,0.062,respectively). Conclusions Cis-platin can induce the apoptosis on HCT116 cells and thus inhibit the reproduction of tumor cells by recovering the function of p.53.
