Please use this identifier to cite or link to this item:
|Title:||Id-1 stimulates serum independent prostate cancer cell proliferation through inactivation of p16INK4a/pRB pathway|
|Authors:||Ouyang, XS;Wang, X;Ling, MT;Wong, HL;Tsao, SW;Wong, YC|
|Publisher:||Oxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/|
|Description:||It has been suggested that the helix-loop-helix protein Id-1 plays an important role in tumourigenesis in certain types of human cancer. Previously, we reported that Id-1 was up-regulated during sex hormone-induced prostate carcinogenesis in a Noble rat model (Ouyang et al. (2001) Carcinogenesis, 22, 965-973). In the present study, we investigated the direct effect of Id-1 expression on human prostate cancer cell proliferation by transfecting an Id-1 expression vector into a prostate cancer cell line LNCaP. Ten stable transfectant clones were isolated and the ectopic Id-1 expression resulted in both increased DNA synthesis rate and the percentage of S phase cells. To study the possible mechanisms involved in the Id-1 induced prostate cancer cell growth, we examined the expression of several factors responsible for G1 to S phase progression. We found that Id-1 expression induced phosphorylation of RB and down-regulation of p16INK4a but not p21Waf1 or p27Kip1. Our results indicate that the Id-1 induced inactivation of p16INK4a/pRB pathway may be responsible for the increased cell proliferation in prostate cancer cells. Given the fact that both Id-1 over-expression and inactivation of p16INK4a/ pRB are common events in prostate cancer, our results provide a possible mechanism on the molecular basis of prostate carcinogenesis.|
|Standard no:||Carcinogenesis, 2002, v. 23 n. 5, p. 721-725|
|Appears in Collections:||Department of Anatomy|
Files in This Item:
Click on the URI links for accessing contents.
Items in HannanDL are protected by copyright, with all rights reserved, unless otherwise indicated.