The Study On The Biological And Chemoresistance Characteristic Of Hepatoma Subgroup With High Proliferation Ability In Rats

Objective: To search for the different proliferation ability subgroup cells in hepatocarcinoma and study the biological and chemoresistance characteristic of the subpopulation cells with high proliferation ability in rats. Methods:(1) The primary liver carcinoma was induced by diethylnitrosamine in rats. We separated the subgroup cells with high ability of proliferation by monoclone culture. Then study the morphous characteristic, proliferation ability, tumoriganic ability and differentiation potency of the subgroup cells. (2) The common tumor cells and HSG-2 from 6 hepatocarcinoma rats were separated .The. inhibition ratio of Adriacin(0.2μg/ml, 72h),Cisplatin (1μg/ml, 72h) and Fliorouracil(5μg/ml, 72h) to common tumor cells and HSG-2 were measured by SRB way. Result: (1) 2 different subgroup were found which can proliferated continuous when were cultured in 6 rats, which were named as HSG1 and HSG2. (2)The doubling generation time and the maximum proliferation multiple and the cell cycle distribution of HSG-2 had significant difference from that of HSG1. (3) HSG2 had a high tumoriganic ratio when were injected to nude mice, which were 100%(6/6) for original density inoculation and 50%(3/6) for 1/10 of original density inoculation. The tumoriganic ratio of HSG2 was higher than the HSG1,which was 0%(0/6)[ P=0.001, original density inoculation; P=0.0231/10 of original density inoculation].(4) When was cultured for long time, the HSG2 can differentiated into HSG1 and HSG2.The offspring HSG2 had strong tumoriganic ability too. But the HSG1 can not differentiated into HSG2. The offspring of HSG1 still had not any tumoriganic ability. (5) The inhibition ratio of Adriacin,Cisplatin and Fliorouracil to HSG-2 were different from that of the common tumor cells, which were [t=4.321, P=0.002], [t=4.965, P=0.001] and [t=4.285, P=0.002].(6) The IC50 of Adriacin,Cisplatin and Fliorouracil to HSG-2 were different from that of the common tumor cells, which were [t=10.604, P＜0.001], [t=5.642, P＜0.001] and [t=9.470, P＜0.001]. Conclusion: HSG2, which had low growth rate in vitro, stronger tumoriganic ability and the potency of differentiation, exhibited the characters of TSC. The inhibition ability of anticancer drugs to HSG2 was lower than that it to the common hepatocarcinoma cells. It suggested that the HSG-2 had a distinct chemoresistance mechanism like the tumor stem cells.