Abstract

Background: The p73 gene is a p53 homologue that induces apoptosis and inhibits cell proliferation. N-terminal truncated isoforms of p73 (ΔNp73) act as dominant-negative inhibitors of wild-type p53 and TAp73 and result in tumour growth in nude mice.

Aims: To detect ΔNp73 expression in 24 benign prostatic hyperplasia samples, 33 prostate carcinomas, and five normal samples and to evaluate the relation between ΔNp73, TAp73 concentrations, and the clinicopathological characteristics of patients with prostate cancer.

Methods: TAp73 was determined by real time polymerase chain reaction (PCR); ΔNp73 and ΔN’p73 were assessed using reverse transcription PCR. western blotting was used to analyse protein expression. p53 mutation was determined by immunohistochemistry.

Results: A significant increase of ΔNp73 was seen in 20 of 33 carcinomas and 17 of 24 benign prostate hyperplasia tissues, but in none of the normal samples. None of the specimens expressed ΔN’p73. No significant relation was found between TAp73 expression and clinical parameters. The incidence of positive expression of ΔNp73 correlated with the Gleason score in prostate carcinomas. Cancer samples with wild-type p53 had significantly higher expression of ΔNp73 than p53 mutant cancers.

Conclusion: These data suggest a potential role for ΔNp73 in prostate cancer progression.