VPS33B对卵巢癌细胞增殖凋亡的影响及机制研究

Effect of VPS33b on proliferation and apoptosis of ovarian cancer cells and its mechanism

目的:研究VPS33B对卵巢癌细胞增殖凋亡的影响及机制,旨在为卵巢癌的诊治提供新的思路和靶点。方法:选择人卵巢癌OVACA-3细胞进行研究。按照处理方式的差异分成三组,即过表达VPS33B组、干扰VPS33B过表达组以及OVACA-3对照组。其中过表达VPS33B组予以VPS33B过表达慢病毒转染处理,干扰VPS33B过表达组予以干扰VPS33B过表达慢病毒转染处理,OVACA-3对照组不予以任何转染处理。分析三组细胞增殖情况、凋亡情况以及磷脂酰肌醇3-激酶(PI3K)、蛋白激酶B(AKT)、c-Myc蛋白表达水平的差异。结果:过表达VPS33B组OVACA-3细胞增殖能力低于OVACA-3对照组和干扰VPS33B过表达组,且干扰VPS33B过表达组OVACA-3细胞增殖能力高于OVACA-3对照组,差异有统计学意义(均P<0.05)。过表达VPS33B组OVACA-3细胞转染48 h后活细胞占比低于OVACA-3对照组和干扰VPS33B过表达组,凋亡细胞、坏死细胞占比高于OVACA-3对照组和干扰VPS33B过表达组;且干扰VPS33B过表达组OVACA-3细胞转染48 h后活细胞占比高于OVACA-3对照组,凋亡细胞、坏死细胞占比低于OVACA-3对照组,差异有统计学意义(均P<0.05)。过表达VPS33B组PI3K、AKT、c-Myc蛋白表达明显低于OVACA-3对照组以及干扰VPS33B过表达组,且干扰VPS33B过表达组PI3K、AKT、c-Myc蛋白表达均高于OVACA-3对照组,差异有统计学意义(均P<0.05)。结论:VPS33B对卵巢癌细胞增殖具有一定的抑制作用,同时对卵巢癌细胞凋亡具有促进作用,其主要作用机制可能与抑制PI3K/AKT/c-Myc信号通路活性有关。

Objective To study the effect of VPS33b on the proliferation and apoptosis of ovarian cancer cells and to analyze the mechanism,in order to provide new ideas and targets for the diagnosis and treatment of ovarian cancer.Method Human ovarian cancer Ovaca-3 cells were selected for the study.According to the difference of treatment methods,they were divided into 3 groups,namely,overexpression group of VPS33B,interference group of overexpression of VPS33B and control group of OVACA-3.The overexpressed VPS33B group was transfected with the overexpressed VPS33B lentivirus,the overexpressed interference VPS33B group was transfected with the overexpressed VPS33B lentivirus,and the Ovaca-3 control group was not transfected with any treatment.The cell proliferation,apoptosis and the protein expression levels of PI3K,AKT and c-myc in the three groups were analyzed.Results The proliferation ability of Ovaca-3 cells in the overexpressed VPS33B group was lower than that in the control group and the overexpressed VPS33B group,and the proliferation ability of Ovaca-3 cells in the overexpressed VPS33B group was higher than that in the control group(all P<0.05).After transfection for 48h,the proportion of living cells in Ovaca-3 overexpressed VPS33B group was lower than that in Ovaca-3 control group and interference VPS33B overexpression group,and the proportion of apoptotic cells and necrotic cells was higher than that in Ovaca-3 control group and interference VPS33B overexpression group.After transfection 48 h,the proportion of living cells in Ovaca-3 group was higher than that in Ovaca-3 control group,and the proportion of apoptotic cells and necrotic cells was lower than that in Ovaca-3 control group(all P<0.05).The protein expressions of PI3K,Akt and c-myc in the overexpressed VPS33B group were significantly lower than those in the Ovaca-3 control group and the overexpressed interference VPS33B group,and the protein expressions of PI3K,Akt and c-myc in the overexpressed interference VPS33B group were higher than those in the Ovaca-3 control group(all P<0.05).Conclusion VPS33B can inhibit the proliferation of ovarian cancer cells and promote the apoptosis of ovarian cancer cells,and the main mechanism of action may be related to the inhibition of PI3K/Akt/c-myc signaling pathway activity.