BACKGROUND & OBJECTIVE: Some studies have showed that autophagy suppression may result in malignant transformation, and the inactivation of autophagy gene Beclin1 induces malignancy. This study was to investigate the role of Beclin1 in the tumorigenesis and development of epithelial ovarian carcinoma, and to explore the effect of Beclin1 overexpression on the growth of ovarian carcinoma cell line SKOV3 in vitro. METHODS: The expression of Beclin1 in 25 specimens of normal ovarian tissue, 25 specimens of benign ovarian neoplasia, 19 specimens of borderline ovarian tissue, and 69 specimens of epithelial ovarian carcinoma was detected by immunohistochemistry. Eukaryotic expression vector pcDNA3.1/Beclin1 was constructed and transfected into SKOV3 cellsû plasmid pcDNA3.1 was used as control. The effect of Beclin1 overexpression on the proliferation of SKOV3 cells was evaluated by MTT assay. Cell apoptosis was measured by flow cytometry (FCM). RESULTS: The expression of Beclin1 was high in normal and benign ovarian neoplasia tissues, and there was no significant difference between the 2 groups (P>0.05). Reduced Beclin1 expression was observed in borderline lesions, and the lowest level was detected in ovarian carcinoma tissues (P<0.05). The inhibition rate was significantly higher in pcDNA3.1/Beclin1-SKOV3 cells than in pcDNA3.1-SKOV3 cells [(68.75+/-5.10)% vs. (10.91+/-4.20)%, P<0.05]. At 72 h after transfection, the apoptosis rate was significantly higher in pcDNA3.1/Beclin1-SKOV3 cells than in pcDNA3.1-SKOV3 cells and SKOV3 cells [(19.07+/-0.65)% vs. (4.30+/-0.50)% and (3.87+/-0.84)%, P<0.05]. CONCLUSIONS: Beclin1 expression is down-regulated in epithelial ovarian cancer tissues, which may relate to tumorigenesis and development of epithelial ovarian cancer. Beclin1 overexpression can inhibit proliferation and induce apoptosis of SKOV3 cells.
BACKGROUND & OBJECTIVE: Some studies have showed that autophagy suppression may result in malignant transformation, and the inactivation of autophagy gene Beclin1 induces malignancy. This study was to investigate the role of Beclin1 in the tumorigenesis and development of epithelial ovarian carcinoma, and to explore the effect of Beclin1 overexpression on the growth of ovarian carcinoma cell line SKOV3 in vitro. METHODS: The expression of Beclin1 in 25 specimens of normal ovarian tissue, 25 specimens of benign ovarian neoplasia, 19 specimens of borderline ovarian tissue, and 69 specimens of epithelial ovarian carcinoma was detected by immunohistochemistry. Eukaryotic expression vector pcDNA3.1/Beclin1 was constructed and transfected into SKOV3 cellsû plasmid pcDNA3.1 was used as control. The effect of Beclin1 overexpression on the proliferation of SKOV3 cells was evaluated by MTT assay. Cell apoptosis was measured by flow cytometry (FCM). RESULTS: The expression of Beclin1 was high in normal and benign ovarian neoplasia tissues, and there was no significant difference between the 2 groups (P>0.05). Reduced Beclin1 expression was observed in borderline lesions, and the lowest level was detected in ovarian carcinoma tissues (P<0.05). The inhibition rate was significantly higher in pcDNA3.1/Beclin1-SKOV3 cells than in pcDNA3.1-SKOV3 cells [(68.75+/-5.10)% vs. (10.91+/-4.20)%, P<0.05]. At 72 h after transfection, the apoptosis rate was significantly higher in pcDNA3.1/Beclin1-SKOV3 cells than in pcDNA3.1-SKOV3 cells and SKOV3 cells [(19.07+/-0.65)% vs. (4.30+/-0.50)% and (3.87+/-0.84)%, P<0.05]. CONCLUSIONS:Beclin1 expression is down-regulated in epithelial ovarian cancer tissues, which may relate to tumorigenesis and development of epithelial ovarian cancer. Beclin1 overexpression can inhibit proliferation and induce apoptosis of SKOV3 cells.