Abstract: Objective To investigate the molecular mechanisms by which sufentanil affects cervical cancer (CC) cells. Methods Real-time quantitative PCR ( RT-qPCR) assay was used todetect the expression level of lncRNA CCAT1 in CC tissues and precancerous tissues, and in the cervical epithelial cells GH329 and CC cell lines (HeLa, CaSki, Siha and C4-1) . Subsequently, CC cells CaSki were randomly divided into 4 groups: blank group, sufentanil group, sufentanil + oe-NC group and sufentanil + CCAT1 group. RT-qPCR assay was then used to examine the expression level of lncRNA CCAT1 in each group. Cell Counting Kit-8 (CCK-8) assay was used to detect the cell proliferation ability. Flow cytometry was used to detect the changes of cell cycle and the cellapoptosis. Results lncRNA CCAT1 was highly expressed in CC tissues and the CC cell lines (HeLa, CaSki, Siha and C4-1) when compared with that in the precancerous tissues and that in theGH329 cells respectively (P < 0. 01) . The expression level of lncRNA CCAT1 in and the proliferation ability of CaSki cells were significantly decreased (P < 0. 01), while the proportion of cells in the G 0 / G1 phase and the apoptosis rate were significantly increased (P<0. 01) in the sufentanil groupwhen compared with those in the blank group. The expression level of lncRNA CCAT1 and the proliferation ability of CaSki cells in the sufentanil + oe-CCAT1 group were significantly increased (P < 0. 01), while the proportion cells in the G0 / G1 phase and cell apoptosis rate were significantly decreased (P<0. 01) when compared with those in the sufentanil + oe-NC group. Conclusion Sufentanil could blockthe CC cell cycle by decreasing lncRNA CCAT1 expression in CC cells, ultimately inhibiting the proliferative ability of CC cells and promoting cell apoptosis.

Key words: