Objective To investigate the effect mechanism of sanguinarine on the proliferation,apoptosis,invasion and migration abilities of cervical cancer cells.Methods MTT,flow cytometer,cell scratch test and Transwell chamber assay were respectively used to detect the cellular proliferation,apoptosis,migration and invasion abilities after sanguinarine action.The expression levels of E-Cadherin,PTEN,β-catenin and MMP2 protein of cervical cancer cells after sanguinarine action were detected by Western blot.Results 0.6,0.8 μmol/L sanguinarine had the inhibitory effect on the proliferation of cervical cancer cells.After 0.8μmol/L sanguinarine action for 48 h,cervical cancer HeLa and Siha cells apoptosis rate were up to (45.68± 2.26)％ and(31.89 ± 3.80)％ respectively.0.8 μmol/L sanguinarine action for 3 h,cervical cancer cells HeLa and Siha adhesion rates were only (67.45 ± 2.13)％and(73.59± 2.61)％.0.8 mol/L sanguinarine action for 16 h,the invasion numbers of cervical cancer Hela and Siha cell were (39.64 ±1.98) and (43.87 ± 2.83) respectively.The expression amount of E-Cadherin and PTEN in cervical cancer cells after sanguinarine action was increased,while the expression amount of E-Cadherin and PTEN was weakened.Conclusion Sanguinarine has the proliferation inhibiting and apoptosis promoting effect on cervical cancer cells,its mechanism may be related to adhesion protein E-Cadherin,β-catenin and PTEN,MMP2.

Objective: To explore the action mechanism of miR-139-5p inhibiting proliferation and invasion of epithelial ovarian cancer (EOC) cells by targetedly regulatingNotch1.Methods: A total of 24 pairs of EOC tissues and its corresponding para-cancerous tissues from patients, who underwent surgical resection in the DepartmentofGynecology,Nanyang Central Hospital of Henan Province, were collected for this study; in addition, human ovarian cancer cell lines (SKOV3, ES2, HEY-T30) and human ovarian epithelial cell line IOSE80 were also collected. Real-time quantitative PCR (qPCR) was applied to detectmRNAexpressionofmiR-139-5pandNotch1 in EOC tissues and cell lines. The miR-139-5p over-expression vector and recombinant plasmid pLV-Notch1 were transfected into SKOV3 cells. Blank control group (Ctrl group) and negative control group (NC group) were set up. Dual luciferase reporter gene assay was applied to verify the targeting relationship between miR-139-5p and Notch1 3'-UTR. CCK-8, Transwell and Scratch healing experiments were applied to detect cell proliferationinvasionandmigration, respectively. Western blotting was applied to detect expressions of proliferation and migration related proteins in cells. Results: Compared with para-cancerous tissues and IOSE80 cells, the expression of miR-139-5p was significantly decreased in EOC tissues and cell lines, while the expression of Notch1 mRNA was significantly increased (all P<0.01). The results of Dual luciferase reporter showed that Notch1 was the downstream target gene of miR-139-5p. Compared with NC group, cell proliferation, invasion and migration ability, expression levels of Notch1, NICD, Cyclin D1, Cyclin A1, Snail1, β-catenin and N-cadherin were all significantly decreased on 3 d in miR-139-5p mimic group (all P<0.01), while expression of E-cadherin was significantly increased (P<0.01); meanwhile, over-expression of Notch1 could reverse the inhibitory effect of miR-1395p on proliferation, invasion and migration of SKOV3 cells. Conclusion: miR-139-5p can targetedly regulate Notch1 to inhibit proliferation, invasion and migration of EOC cells, which may be related to its down-regulation of NICD, Cyclin D1, Cyclin A1, Snail1, βcatenin and N-cadherin, and up-regulation of E-cadherin.