Invitrostudy of hydrogen sulfide inhibits proliferation and invasion of prostate cancer bone metastasis PC-3 cells

Objective To investigate the effect of hydrogen sulfide on prostate cancer bone metastasis PC-3 cells pro liferation and invasion in vitro and the possible mechanism.Methods PC-3 cells were treated with NaHS(a donor of hydrogen sulfide) at 0,1,2,4 mmol/L concentration for 36 h,respectively,then cell viability was tested by cell counter kit-8.Transwell assay were used to detect PC-3 cells invasive ability and ELISA was used to detect MMP-2 and MMP-9 secretion.PC-3 cells were treated with NaHS at 0,1,2,4 mmol/L concentration for 36 h,then the ex pressions of Bcl-2,Bax were evaluated by Western-Blot assay.Results The effects of hydrogen sulfide on PC-3 cells proliferation: the differences of cell viabilitie were not significant(P 0.05) when PC-3 cells were treated with NaHS at 1 mmol/L concentrations.When PC-3 cells were treated with NaHS at 2,4 mmol/L concentration,the cell viability was declined,compare with control group(P 0.05,P 0.01).The effects of hydrogen sulfide on PC-3 cells invasive: the numbers of transfer to the other side of transwell membrane were counted in tumor invasive assay.The difference of 1 mmol/L NaHS group was not significant compared with control group(P 0.05) and 2 mmol/L NaHS group and 4 mmol/L NaHS group were declined compared with control group(P 0.05 or P 0.01).The effect of hydrogen sulfide on MMP-2 and MMP-9 secretion: when cells were treated by 1 mmol/L NaHS,the secretion of MMP-2 and MMP-9 was not significant compared with control group(P 0.05),2 mmol/L NaHS group and 4 mmol/L NaHS group were declined of MMP-2 and MMP-9 secretion compared with control group(P 0.05 or P 0.01).The effects of hydrogen sulfide on PC-3 cells Bcl-2 and Bax expression: the expression of Bcl-2 was declined and Bax expression in creased compare with control group.Conclusion Hydrogen sulfide can inhibit the growth and invasive of PC-3 cells at the concentration 2,4 mmol/L by affecting Bcl-2 and Bax expression and reducing secretion of MMP-2 and MMP-9.