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Carcinogenesis, Vol. 23, No. 5, 721-725, May 2002
© 2002 Oxford University Press

CANCER BIOLOGY

Id-1 stimulates serum independent prostate cancer cell proliferation through inactivation of p16INK4a/pRB pathway

Xue Song Ouyang, Xianghong Wang, Ming-Tat Ling, Hing Lok Wong, Sai Wah Tsao and Y.C. Wong,1

Department of Anatomy, Faculty of Medicine, 5/F, Li Shu Fan Building, 5 Sassoon Road, University of Hong Kong, Hong Kong, SAR, China

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 p21Waf1or 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.


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