37 research outputs found
Pioglitazone counteracts the tumor necrosis factor-α inhibition of follicle-stimulating hormone-induced follicular development and estradiol production in an in vitro mouse preantral follicle culture system
Effects of Different Trehalose Concentrations in a Warming Medium on Embryo Survival and Clinical Outcomes in Vitrified Human Embryos
Bezafibrate Restores the Inhibition of FSH-Induced Follicular Development and Steroidogenesis by Tumor Necrosis Factor-Alpha Through Peroxisome Proliferator-Activated Receptor-Gamma Pathway in an In Vitro Mouse Preantral Follicle Culture1
Study of the growth factors for the mammary gland: Epidermal growth factor and mesenchyme-derived growth factor
Differential regulation of the inducible nitric oxide synthase gene by estrogen receptors 1 and 2
The Wilms' Tumor Gene WT1 −17AA/−KTS Splice Variant Increases Tumorigenic Activity Through Up-Regulation of Vascular Endothelial Growth Factor in an In Vivo Ovarian Cancer Model
The Wilms' tumor 1 gene WT1 encodes a zinc transcription factor involved in a variety of cancer-related processes. In this study, we sought to investigate the effects of WT1 splice variants on tumorigenic activity and survival in an in vivo ovarian cancer model. To this end, we established stable ovarian cancer cell lines transduced with lentiviral constructs containing each of the four WT1 splice variants (−17AA/−KTS, +17AA/−KTS, −17AA/+KTS, and +17AA/+KTS). In mice inoculated intraperitoneally with SKOV3ip1 cells expressing WT1 −17AA/−KTS, disseminated tumor weights and production of ascites were significantly increased compared with those in mice inoculated with cells expressing the control vector. The overall survival in mice inoulated with WT1 −17AA/−KTS-expressing cells was significantly shorter than that in mice inoculated with control cells (P = .0115). Immunoblot analysis revealed that WT1 −17AA/−KTS significantly increased the expression of vascular endothelial growth factor (VEGF) compared with the control. Greater numbers of CD31-immunopositive vessels were observed in tumors from mice injected with cells expressing WT1 −17AA/−KTS than in tumors from control mice. Finally, WT1 −17AA/−KTS significantly increased tumor microvessel density compared with that in the control (P < .05). Treatment with anti-VEGF antibody (bevacizumab) inhibited tumor growth, dissemination, and ascites production in mice injected with cells expressing WT1 −17AA/−KTS. The overexpression of WT1 −17AA/−KTS induced a more aggressive phenotype in ovarian cancer cells through VEGF up-regulation in an in vivo ovarian cancer model. Our findings indicated that WT1 −17AA/−KTS enhanced tumorigenic activity and could decreased patient survival through up-regulation of VEGF expression in ovarian cancers