棕榈酸在体外通过促进凋亡作用抑制宫颈癌Hela细胞增殖的研究

Palmitate inhibits proliferation of cervical cancer Hela cells by promoting apoptosis

目的探讨体外棕榈酸(Palmitic acid,PA)抑制人宫颈癌HeLa细胞增殖、迁移、侵袭和诱导凋亡作用及其部分机制。方法体外培养的宫颈癌HeLa细胞分为对照组(不加药)、PA处理组(分别加入PA 25、50、100μg/mL处理),CCK-8法检测各组HeLa细胞增殖情况,Transwell试验检测细胞的迁移和侵袭能力,qRT-PCR检测不同浓度PA处理后细胞凋亡相关基因Bcl-2、Bax及Cleaved-caspase-3的表达,PA处理后的HaLa细胞用膜联蛋白V/碘化丙啶双标,随后用流式细胞仪检测其凋亡情况。结果与对照组比较,PA处理HeLa细胞后增殖抑制率逐渐增高(P<0.05);PA处理后,HaLa细胞的迁移与侵袭能力显著下降(P<0.05);同时,PA处理HeLa细胞后,随着PA浓度增高,Bcl-2基因表达逐渐降低,而Bax和Cleaved-caspase-3基因表达逐渐增强与流式细胞仪检测结果相符合,HeLa细胞的凋亡率随着PA浓度增高逐渐增高(P<0.05)。结论PA体外可抑制HeLa细胞增殖,减少其迁移与侵袭水平,并诱导其凋亡,其机制可能与调节HeLa细胞Bcl-2家族有关。

Objective The aim of this study was to investigate the inhibitory effects of palmitic acid(PA)on proliferation,migration,invasion and apoptosis of human cervical carcinoma Hela cells and its mechanism.Methods Hela cells cultured in vitro were divided into the control group(without PA)and PA treatment group(25,50,100 μg/mL of PA).CCK-8 assay was used to detect the ability of proliferation in Hela cells in each group.The abilities of migration and invasion were detected in Hela cells by the Transwell assay.After treatment with different concentrations of PA,RT-qPCR was used to detect the expression of apoptosis-related genes including bcl-2,bax and cleaved-caspase-3.Flow cytometry were used to detect apoptosis of Hela cells double-labeled with annexin V/propidium iodide.Results Compared with the control group,the inhibitory proliferative rates of Hela cells treated with PA increased gradually( P <0.05).After PA treatment,the abilities of migration and invasion in Hala cells significantly decreased( P <0.05).At the same time,after treatment with PA,the expression of bcl-2 gene was decreased gradually,and the expression of bax and cleaved-caspase-3 genes were gradually increased.The apoptosis rates of Hela cells treated with PA increased in a dose-dependent manner( P <0.05).Conclusion PA can inhibit proliferation,reduce migration and invasion,and induce apoptosis of Hela cells,which may be related to the regulation of bcl-2 family in HeLa cells.