不同浓度的依托咪酯通过调控FEZF1-AS1的表达对结直肠癌细胞生物学功能的影响

Impacts of different concentrations of etomidate on the biological function of colorectal cancer cells by regulating the expression of FEZF1-AS1

目的探讨不同浓度依托咪酯对结直肠癌细胞生物学功能的影响,并分析其潜在机制。方法使用0、4、16、64μmol/L依托咪酯分别处理结直肠癌细胞(LS513细胞)48 h,测定细胞存活率、凋亡率、迁移侵袭能力,并检测Bcl-2、BAX、Cleaved caspase-3及LncRNA FEZF1-AS1和miR-363-3p的表达水平。培养LS513细胞,分为三组:空白组、依托咪酯64μmol/L组、pcDNA-FEZF1-AS1组。比较三组细胞生物学功能。结果4、16、64μmol/L依托咪酯处理LS513细胞后,细胞存活率、迁移细胞数、侵袭细胞数均降低,凋亡率增加,且凋亡相关蛋白Cleaved caspase-3、Bax表达升高,Bcl-2表达降低(P<0.05);过表达LncRNA FEZF1-AS1后,LS513细胞LncRNA FEZF1-AS1表达升高,miR-363-3p表达降低,且过表达LncRNA FEZF1-AS1后LS513细胞存活率、迁移细胞数及侵袭细胞数升高,凋亡率降低(P<0.05)。结论依托咪酯可抑制结直肠癌细胞迁移、侵袭,并促进其凋亡,且可能通过调控LncRNA FEZF1-AS1/miR-363-3p信号轴发挥作用。

Objective To investigate the impacts of different concentrations of etomidate on the biological function of colorectal cancer cells,so as to analyze its potential mechanism.Methods 0,4,16 and 64μmol/L etomidate were used to treat colorectal cancer cells(LS513 cells)for 48 hours,the cell survival rate and apoptosis rate were determined,and the expression levels of Bcl-2,BAX,Cleaved caspase-3,LncRNA FEZF1-AS1 and miR363-3p were detected.The cultured LS513 cells were divided into the blank group,the 64μmol/L etomidate group and the pcDNA-FEZF1-AS1 group.The biological functions of the three groups of cells were compared.Results After treating LS513 cells with etomidate at 4,16,64μmol/L,the cell survival rate,the number of migrating cells and the number of invading cells all decreased,the apoptosis rate increased,and the expression of apoptosis-related proteins Cleaved caspase-3 and Bax increased,while the expression of Bcl-2 decreased(P<0.05).After overexpression of LncRNA FEZF1-AS1 in LS513 cells,the expression of LncRNA FEZF1-AS1 increased,and the expression of miR-363-3p decreased.In addition,after overexpression of LncRNA FEZF1-AS1,the survival rate,the number of migrating cells and the number of invading cells increased and the apoptosis rate decreased(P<0.05).Conclusion Etomidate can inhibit the migration and invasion of colorectal cancer cells,and promote their apoptosis,and may play a role by regulating LncRNA FEZF1-AS1/miR-363-3p signal axis.