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Carcinogenesis Advance Access published online on April 1, 2004
Carcinogenesis, doi:10.1093/carcin/bgh154
© 2004 by Oxford University Press
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© 2004 Oxford University Press

CARCINOGENESIS

Overexpression of tumour suppressor retinoblastoma 2 protein (pRb2/p130) in hepatocellular carcinoma

Hung Huynh 1*

1 Laboratory of Molecular Endocrinology, Division of Cellular and Molecular Research, National Cancer Centre of Singapore, Singapore 169610

* Corresponding author. E-mail: cmrhth{at}nccs.com.sg.

Received 21 October 2003 ; revised 10 March 2004 ; accepted 22 March 2004

Abstract

Hepatocellular carcinoma (HCC) is one of the most common malignancies in Southeast Asia. Although inactivation of pRb2/p130 has been reported in variety of human cancer, its function in HCC has not been established. In this study we report that loss of expression of pRb2/p130 was detected by immunohistochemistry and Western blotting in 15.2% (7 of 46) HCCs examined. High levels of pRb2/p130 expression were found in 84.8% (39 of 46) HCCs studied. Western blot analysis revealed that HCC had 3.5-fold higher pRb2/p130 than ABL tissues. 71.7% (33 of 46) of HCCs examined exhibited both nuclear and cytoplasmic staining for pRb2/p130. Cytoplasmic staining was found in 93.5% (43 of 46) of adjacent benign liver tissues. Overproduction of pRb2/p130 in HepG2 cells led to growth suppression, cell cycle arrest a G0/G1, altered cell morphology, inhibition of in vitro colony formation and reduction in tumourigenicity in SCID mice. This demonstration provides the role of pRb2/p130 as a tumour suppressor protein in HCC and the loss of this protein may lead to the development or progression of HCC. Overexpression of pRb2/p130 in HCC was, therefore, suggested to be a programmed protective response of the organism to uncontrolled proliferation.

HCC, pRb2/p130, tumour suppressor
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