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 购宝钱包 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 购宝钱包 s (androgen dependent [AD] prostate cancer 购宝钱包 line) stimulated 购宝钱包 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 购宝钱包 s also resulted in reducing the sensitivity of prostate cancer 购宝钱包 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 购宝钱包 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.