Lidocaine inhibits cervical cancer cell proliferation and induces cell apoptosis by modulating the lncRNA-MEG3/miR-421/BTG1 pathway.

This study aimed to explore the effect of lidocaine on the growth of cervical cancer cells (HeLa) and the underlying molecular mechanisms. Cell counting kit-8 (CCK-8) and flow cytometry (FCM) were used to detect the cell viability and apoptosis of cervical cancer cells after lidocaine treatment. Lidocaine inhibited cell viability and promoted apoptosis in HeLa cells. Long noncoding RNA maternally expressed gene 3 (lncRNA-MEG3) was significantly downregulated in cervical cancer cells, and lidocaine increased the expression of lncRNA-MEG3 in HeLa cells. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR), CCK-8, and FCM assays were used to test indicators. MEG3-shRNA promoted the cell viability and inhibited apoptosis, while the effect of lidocaine was the opposite. The effects of lidocaine on HeLa cells were reversed by MEG3-shRNA. The level of miR-421 in cervical cancer and normal cervical cells was detected using qRT-PCR. The MEG3-plasmid could inhibit cell viability and induce cell apoptosis, but these effects were reversed by miR-421 upregulation. Hence, lidocaine suppressed tumor growth by regulating cell viability and inducing apoptosis. The results indicated that BTG anti-proliferation factor 1 (BTG1) was a direct target of miR-421. HeLa cells were transfected with inhibitor control, miR-421 inhibitor, control-shRNA, or BTG1-shRNA. The negative effects of the miR-421 inhibitor or knockdown BTG1 on cell viability and apoptosis were identified using CCK-8 assay and FCM. The miR-421 inhibitor improved cervical cancer progression by regulating BTG1 expression. The results suggested that lidocaine inhibited the growth of cervical cancer cells by modulating the lncRNA-MEG3/miR-421/BTG1 signaling pathway, providing opportunities for treating cervical cancer.