Abstract: BTG (B-cell translocation gene) can inhibit cell proliferation, metastasis, and angiogenesis and regulate cell cycle progression and differentiation in a variety of cell types. We aimed to clarify the role of BTG1 in ovarian carcinogenesis and progression. A BTG1-expressing plasmid was transfected into ovarian carcinoma cells and their phenotypes and related proteins were examined. BTG1 mRNA expression was detected in ovarian normal tissue (n = 17), ovarian benign tumors (n = 12), and ovarian carcinoma (n = 64) using real-time RT-PCR. Ectopic BTG1 expression resulted in lower growth rate, high cisplatin sensitivity, G1 arrest, apoptosis, and decreased migration and invasion. Phosphoinositide 3-kinase, protein kinase B, Bcl-xL, survivin, vascular endothelial growth factor, and matrix metalloproteinase-2 mRNA and protein expression was reduced in transfectants as compared to control cells. There was higher expression of BTG1 mRNA in normal tissue than in carcinoma tissue (p = 0.001) and in benign tumors than in carcinoma tissue (p = 0.027). BTG1 mRNA expression in International Federation of Gynecology and Obstetrics (FIGO) stage I/II ovarian carcinomas was higher than that in FIGO stage III/IV ovarian carcinomas (p = 0.038). Altered BTG1 expression might play a role in the pathogenesis and progression of ovarian carcinoma by modulating proliferation, migration, invasion, the cell cycle, and apoptosis.
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Zhao, Y.; Gou, W.-F.; Chen, S.; Takano, Y.; Xiu, Y.-L.; Zheng, H.-C. BTG1 Expression Correlates with the Pathogenesis and Progression of Ovarian Carcinomas. Int. J. Mol. Sci. 2013, 14, 19670-19680.
Zhao Y, Gou W-F, Chen S, Takano Y, Xiu Y-L, Zheng H-C. BTG1 Expression Correlates with the Pathogenesis and Progression of Ovarian Carcinomas. International Journal of Molecular Sciences. 2013; 14(10):19670-19680.
Zhao, Yang; Gou, Wen-Feng; Chen, Shuo; Takano, Yasuo; Xiu, Yin-Ling; Zheng, Hua-Chuan. 2013. "BTG1 Expression Correlates with the Pathogenesis and Progression of Ovarian Carcinomas." Int. J. Mol. Sci. 14, no. 10: 19670-19680.