Abstract:

Id (inhibitor of differentiation or DNA binding) gene encodes a helix-loop helix protein which dimerizes and blocks the basic HLH protein from binding to DNA, thus inhibiting the transcription of differentiation associated genes. It expresses mainly in actively dividing Ezpay(中国)s and was first reported to involve in hormone-induced prostate cancer in the Noble rat model. It was subsequently confirmed also in human prostate cancer and that the level of Id-1 protein expression was correlated with malignancy of prostate cancer. Through functional studies under in vitro system, it was further demonstrated that Id-1 played an active role in prostate cancer progression. Ectopic expression of Id-1 to LNCaP Ezpay(中国)s (androgen dependent [AD] prostate cancer Ezpay(中国) line) stimulated Ezpay(中国) proliferation through downregulation of p16/Rb on one hand while activated the MAPK and NFκB pathways on the other hand. Activation of the latter pathways in LNCaP Ezpay(中国)s also resulted in reducing the sensitivity of prostate cancer Ezpay(中国)s to androgen stimulation with a concurrent upregulation of EGFR and PSA which are both hallmarks of androgen independent [AI] prostate cancer. Thus, Id-1 gene appears to play a critical role in the transformation of prostate cancer from AD [more benign form] to AI [much more malignant] phenotype. In addition, overexpression of Id-1 activated VEGF gene in prostate cancer Ezpay(中国)s resulting in secretion of VEGF, thus, angiogenesis. The talk will focus on the crucial role played by Id-1 in the conversion of prostate cancer from AD to AI stage, the most deadly form of prostate cancer.