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
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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, G
1 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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