Apoptosis mechanism of gastric cancer cellSGC-7901 induced by Omphalia lapidescens protein pPeOp
10.3969/j.issn.1001-1978.2017.09.017
- VernacularTitle:雷丸蛋白pPeOp诱导胃癌细胞SGC-7901凋亡机制研究
- Author:
Xiaoya ZHAO
;
Zhongxia LU
;
Lijun DU
;
Haowei LIANG
;
Yitao CHEN
- Keywords:
apoptosis;
caspases;
gastric cancer;
SGC-7901;
mitochondrial apoptosis pathway;
death receptor apoptosis pathway;
Omphalia lapidescens
- From:
Chinese Pharmacological Bulletin
2017;33(9):1271-1277
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the apoptosis mechanism of human gastric cancer cell SGC-7901 induced by Omphalia lapidescens protein pPeOp.Methods CCK-8 and flow cytometry were used to detect the inhibitory effect of different concentrations of pPeOp(30, 60, 90 mg·L-1) on SGC-7901.The mRNA and protein expression of TNF-R1, Fas/FasL, Bcl-2, caspase-3 and caspase-8 were detected by qRT-PCR and Western blot.Results SGC-7901 cells were treated with different concentrations of pPeOp(30, 60, 90 mg·L-1) for 24 h.CCK-8 test showed that there was no significant difference between PVP group and the control group.The survival rate of the 5-Fu group was(53.71±7.34)% (P<0.05).The survival rates of pPeOp group(30, 60, 90 mg·L-1) were(80.95±6.25)%, (53.48±5.70)% and(44.61±6.50)%(r=0.984,P=0.016),respectively.Flow cytometry showed that the apoptosis rate of PVP group had no significant difference with control group, and the apoptosis rate of 5-Fu group was about(39.30±3.34)%(P<0.05).The apoptotic rates of pPeOp group(30, 60, 90 mg·L-1) were(10.90±1.25)%, (28.80±2.70)% and (32.00±3.50)%,respectively(P<0.05).The mRNA and protein expression levels of Bcl-2 were down-regulated,whereas the expression of TNF-R1, Fas/FasL, caspase-3 and caspase-8 were significantly up-regulated(P<0.05).Conclusions pPeOp can significantly inhibit the proliferation of gastric cancer cell line SGC-7901 and induce apoptosis in a dose-dependent manner.Death receptor pathway and mitochondrial pathway may be related to pPeOp-induced apoptosis of gastric cancer SGC-7901.
