目的：探究依托咪酯对宫颈癌HeLa细胞增殖、迁移、侵袭及糖酵解的影响和可能机制。方法：体外培养HeLa细胞，经不同剂量（0、0.2、0.4、0.8 μg·ml^-1）依托咪酯干预后，细胞计数试剂盒-8（CCK-8）实验、克隆形成实验、Transwell实验分别测定细胞增殖抑制率、克隆形成数、迁移细胞数和侵袭细胞数，试剂盒测定葡萄糖消耗量和乳酸产生量，蛋白质印迹实验测定M2型丙酮酸激酶（PKM2）、己糖激酶2（HK2）蛋白表达量，实时荧光定量聚合酶链式反应（RT-qPCR）法测定细胞中SLCO4A1-AS1表达量。同时以正常宫颈细胞株Ect1/E6E7为对照，RT-qPCR法测定宫颈癌HeLa细胞中SLCO4A1-AS1表达量。转染SLCO4A1-AS1小干扰RNA至HeLa细胞或用0.8 μg·ml^-1依托咪酯干预转染SLCO4A1-AS1过表达载体的HeLa细胞后，上述相同方法测定细胞增殖抑制率、克隆形成数、迁移细胞数和侵袭细胞数、葡萄糖消耗量、乳酸产生量及PKM2、HK2蛋白表达量。结果：依托咪酯增加HeLa细胞增殖抑制率，降低细胞克隆形成数、迁移细胞数和侵袭细胞数、葡萄糖消耗量、乳酸产生量及PKM2、HK2蛋白表达量，同时降低细胞中SLCO4A1-AS1表达量。宫颈癌HeLa细胞中SLCO4A1-AS1表达量较Ect1/E6E7细胞升高。干扰SLCO4A1-AS1增加HeLa细胞增殖抑制率，降低细胞克隆形成数、迁移细胞数和侵袭细胞数、葡萄糖消耗量、乳酸产生量及PKM2、HK2蛋白表达量。上调SLCO4A1-AS1逆转依托咪酯对HeLa细胞增殖、迁移、侵袭及糖酵解的影响。结论：依托咪酯可抑制宫颈癌HeLa细胞增殖、迁移、侵袭及糖酵解，其作用机制可能与下调细胞中SLCO4A1-AS1表达有关。

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