ABSTRACT
Objective To study the inhibitory effect of aspirin on proliferation of human hepatocellular carcinoma HepG2 cell line and its possible mechanismt. Methods MTT assay and plate cloning experiments was used to detect proliferation of human hepatoma HepG2 cells. Effects of aspirin on autophagosomes in HepG2 cells were detected by acridine orange fluorescence staining. The expression of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) protein in human hepatocellular carcinoma HepG2 cells was detected by Western blot. Results 10 mmol/L concentration of aspirin could inhibit the proliferation of HepG2 cells, but increase the number of autophagosomes of HepG2 cells, increase AMPK expression, decrease mTOR expression. After combination treatemnt with 40 μmol/L autophagy inhibitor chloroquine (CQ), CQ could enhance the inhibitory effect of 10 mmol/L aspirin on proliferation of human hepatoma HepG2 cells. Conclusion Combination treatment with autophagy inhibitor CQ attenuates 10 mmol/L aspirin-induced autophagy thus enhance its anti-HepG2 effect.
ABSTRACT
Objective The objective of this study was to investigate effects of lycopene(LP) on the proliferation and apoptosis of human hepatocellular carcinoma HepG2 cells and to explore its mechanism.Methods HepG2 cells in logarithmic growth phase were treated with 0,5,10,20 μg/mL of LP and 40 μg/mL of Cisplatin for 48 h.Ten replicates in each dose were designed in this study.After treatments,the cell viability was measured by MTT colorimetric assay.The distribution of cell cycle was detected by flow cytometry(FCM).The mRNA expression of Bax and Bcl-2 were measured by RT-PCR.The expression of Caspase-3 protein was explored by Western blot.Results The inhibition rate of HepG2 cells was significantly increased by 10 μg/mL and 20μ g/mL of LP or 40 μg/mL of cisplatin when compared to the negative control group.The cell cycle of HepG2 cells were arrested at the G0/G1 phase and the apoptosis rate were significantly increased in comparison with the negative control group.The level of Bax mRNA expression was significantly increased and decreased in the expression of Bcl-2 mRNA.They were shown an increasing ratio of Bax/Bcl-2 and up-regulated Caspase-3 protein in HepG2 cells treated with LP.All effects in this study show a dose-dependent manner.Conclusion LP can inhibit the proliferation and promote the apoptosis in HepG2 cells.This mechanism may be contributed to arresting cell cycle and regulating gene expression related to apoptosis.