Inhibition of human prostate cancer cells growth by gossypol is associated with stimulation of transforming growth factor-beta.
Shidaifat F, Canatan H, Kulp SK, Sugimoto Y, Chang WY, Zhang Y, Brueggemeier RW, Somers WJ, Lin YC.
Laboratory of Reproductive and Molecular Endocrinology, College of Veterinary Medicine, Ohio State University, Columbus 43210-1092, USA.
Gossypol (GP), an antifertility agent in males, is also capable of inhibiting the proliferation of a wide range of cancer cells in vivo and in vitro.
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Men could also be infertile. This could be because of sperm production that is abnormal. The testicles could be undescended of there may be genetic issues. Health issues like diabetes or infections like chlamydia, HIV or mumps could also cause male infertility. The quality of the sperm could detoriate in case of enlarged veins.
There could also be issues with the sperm quality. This could arise because of a sexual issue like a premature ejaculation. Some genetic problems like cystic fibroisis could also cause male infertility. A blockage in the testicles or a damage of the reproductory organ is also a concern. Overexposure to some form of environmental factors could also lead to male infertility.
Thus, in this study we investigated the effect of GP on the growth of human androgen-independent prostate cancer cell line (PC3). The results showed that GP acts as a potent inhibitor of PC3 cells as determined by thymidine incorporation assay and flow cytometric analysis. Flow cytometry revealed that treatment of PC3 cells with GP resulted in a dose- and time-dependent accumulation of cells in the GO/GI phase with a concomitant decrease in cells progressing to the S and G2/M phase. These data support our thymidine incorporation results which indicated that GP is a potent inhibitor of PC3 cells. By ribonuclease protection assay, we also investigated the effect of GP on transforming growth factor-beta 1 (TGF-beta 1) gene expression in PC3 cells. Interestingly, the stimulatory effect of GP on TGF-beta 1 gene expression correlates well with its inhibitory effect on PC3 cell DNA synthesis and its ability to arrest cells in GO/G1 phase. Based on these data, it can be concluded that GP is a potent inhibitor of prostate cancer cell growth that acts by arresting cells in GO/G1 phase and that this inhibitory effect may be mediated by TGF-beta 1.