Objective To investigate the mechanism of Mi-362 targeting Six1 inhibiting proliferation and migration of cer-vical cancer cells. Methods The expression levels of microRNA-362 in cervical cancer tissues and adjacent tissues were measured in 142 patients with cervical cancer in our hospital. At the same time,Hela cancer cell group,microRNA-362 mimics group and mi-croRNA-362 inhibitor group were set up to determine the viability of cancer cells,the number of monoclonal formation of cancer cells,the apoptotic rate of cancer cells,cell cycle,the number of perforations,and the levels of microRNA-362 and Six1 in cervical cancer fluid of Hela. Results The expression level of miR-362 in cervical cancer tissue was lower than that in adjacent tissue(P<0. 05). The higher the infiltration of lymphatic vessel space,pathological stage,TNM stage,lymph node metastasis and depth of infil-tration,the lower the expression rate of miR-362(P<0. 05). The OD value and survival rate in the miR-362 mimics group were lower than those in the Hela cancer cells group(P<0. 05),while the OD value and survival rate in the mir-362 inhibitor group were higher than those in the Hela cancer cells group and the miR-362 mimics group(P<0. 05). The number of clones formed in the miR-362 mimics group was lower than that in the Hela cancer cell group(P<0. 05),and the number of clones formed in the miR-362 inhibitor group was higher than that in the Hela cancer cell group and the miR-362 mimimics group(P<0. 05). The apoptotic rate of miR-362 mimics group was higher than that of Hela cancer cell group(P<0. 05),and that of miR-362 inhibitor group was lower than that of Hela cancer cell group and miR-362 mimics group(P<0. 05). The G1 phase in the miR-362 mimics group was higher than that in the Hela cancer cell group(P<0. 05),and the G1 phase in the miR-362 inhibitor group was lower than that in the Hela cancer cell group and the miR-362 mimimics group(P<0. 05). The number of cell membrane penetration in the miR-362 mimics group was lower than that in the Hela cancer group(P < 0. 05),and that in the miR-362 inhibitor group was higher than that in the Hela cancer group and the miR-362 mimimics group(P<0. 05). The expression level of miR-362 in the miR-362 mimics group was higher than that in the Hela cancer cell group(P<0. 05),and the expression level of miR-362 in the miR-362 inhibitor group was lower than that in the Hela cancer cell group and the miR-362 mimics group(P<0. 05). The expression level of Six1 in the miR-362 mimics group was lower than that in the Hela cancer cell group(P<0. 05),and that in the miR-362 inhibitor group was higher than that in the Hela cancer cell group and the miR-362 mimics group(P<0. 05). Conclusion miR-362 plays an important inhibition in the occurrence and development of cervical cancer,and its mechanism is related to the inhibition of prolifer-ation,migration and invasion of cancer cells by microRNA-362 through negative regulation of Six1.

[Abstract] Objective: To investigate the effects of forkhead box transcription factor (FOXK2) overexpression on the proliferation, migration, invasion and adhesion of human ovarian cancer SK-OV-3 cells and its related molecular mechanism. Methods: The open reading frame (ORF) of FOXK2 was cloned into lentivirus expression vector, which was then enveloped in HEK293T cells and transfected into human ovarian cancerSK-OV-3cells.TheoverexpressionefficiencywasdetectedbyqPCRandWesternblotting.Theproliferation, migration, invasion and adhesion of SK-OV-3 cells were detected by CCK-8, Scratch-healing, Transwell and Cell adhesion assays respectively, and the expressions of epithelial-mesenchymal transition (EMT) markers were detected by qPCR. Results: The FOXK2 overexpression vector was constructed successfully and packaged into lentivirus, which was then transfected into SK-OV-3 cells. After transfection, the expression of FOXK2 was significantly increased (P<0.01); the proliferation, migration and invasion of SK-OV-3 cells were significantly reduced while the adhesion ability was significantly increased (P<0.05 or P<0.01); and the expression levels of E-cadherin and β-catenin were significantly increased while that of vimentin and fibronection were significantly decreased (all P<0.01). Conclusion: Overexpression of FOXK2 in SK-OV-3 cells leads to a significant decrease in proliferation, migration and invasion but increase in adhesion. The molecular mechanism may be related to the reversion of the EMT process in tumor cells, suggesting that FOXK2 may be a potential target for the diagnosis and treatment of ovarian cancer.