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Wild-Type
p53 Induces Apoptosis in Hep3B through Up-Regulation of Bax Expression |
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Ragai R. Mitry,
Catherine E. Sarraf, Chuan-Ging Wu, Massimo Pignatelli, and Nagy A. Habib
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Departments
of Surgery (RRM, NAH) and Histopathology (CES, MP), Royal Postgraduate Medical
School, Hammersmith Hospital, London, United Kingdom; and Department of
Experimental Medicine (C-GW), Academic Medical Centre, University of Amsterdam,
Amsterdam, The Netherlands |
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We demonstrated that introduction
and expression of wild-type p53 gene in the human hepatocellular carcinoma
cell line, Hep3B, resulted in up-regulation of both p21WAF1/CIP1 and bax
gene expression and apoptosis. This cell line contains integrated hepatitis
B virus sequences and lacks the expression of both p53 and retinoblastoma
tumor suppressor genes because of deletions. Our results suggest that whereas
an increased level of bax expression mediates apoptosis, an increased level
of p21WAF1/CIP1 expression does not induce arrest of cell growth, presumably
because of the deletion of the retinoblastoma gene. This study also confirms
reported observations that p53 is a tumor suppressor gene, which induces
apoptosis in malignant cells that lack normal p53 activity because of mutation,
deletion, or inactivation of the gene by the presence of oncogenic viral
proteins. |
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