Study on the Functional Effects of Cetuximab on Prostate Cancer PC-3 Cells

Yu Zhuoxuan; Jiang Shuxu; Li Changyi; He Dongyue; He Zhen; Fu Dewang

Abstract：Objective To observe the effects of different concentrations of cetuximab on the proliferation,invasion and apoptosis of prostate cancer PC-3 cells,and to explore its possible mechanism.Methods PC-3 cells were treated with different concentrations of cetuximab(10,20,40,and 80 μg/mL)for 24 h,and CCK-8 was used to detect changes in cell proliferation activity;flow cy-tometry was used to detect changes in cell apoptosis;transwell assay was used to detect the changes in cell invasion ability;RT-PCR was used to detect changes in EGFR mRNA expression;Western Blot was used to detect changes in Bax and Bcl-2 protein expression.Results The CCK-8 results showed that different concentrations of cetuximab could inhibit the cell proliferation activity of PC-3 after 24 hours of action(P<0.001),and the drug's inhibitory effect was dose-dependent on the concentration;the results of apoptosis de-tection showed that different concentrations of cetuximab inhibited the invasive ability of PC-3 cells(P<0.001),and the drug's in-hibitory effect was dose-dependent on the concentration;the apoptosis detection results showed that different concentrations of cetux-imab resulted in an increase in the total apoptosis proportion of PC-3 cells(P<0.01),and this proapoptotic ability was dose-de-pendent on the concentration;Western Blot results showed that different concentrations of cetuximab could inhibit Bc1-2 protein ex-pression(P<0.05)and promote Bax protein expression(P<0.05),and the inhibitory and promoting effects were dose-dependent on drug concentration;the RT-PCR results showed that different concentrations of cetuximab could inhibit EGFR mRNA expression(P<0.05),and the inhibitory effect was also dose-dependent on the drug concentration.Conclusion Cetuximab can inhibit the pro-liferation and invasion of PC-3 in prostate cancer cells and promote cell apoptosis,and this effect may be achieved by inhibiting EGFR signaling pathway leading to cell apoptosis.