Sayan, AE, Sayan, BS 
ORCID: https://orcid.org/0000-0003-2305-1970, Findikli, N and Ozturk, M
2001,
'Acquired expression of transcriptionally active p73 in hepatocellular carcinoma cells'
, Oncogene, 20
, pp. 5111-5117.
Abstract
p53 and p73 proteins activate similar target genes and induce apoptosis and cell cycle arrest. However, p53, but not p73 is considered a tumour-suppressor gene. Unlike p53, p73 deficiency in mice does not lead to a cancer-prone phenotype, and p73 gene is not mutated in human cancers, including hepatocellular carcinoma. Here we report that normal liver cells express only ΔN-p73 transcript forms giving rise to the synthesis of N-terminally truncated, transcriptionally inactive and dominant negative p73 proteins. In contrast, most hepatocellular carcinoma cells express TA-p73 transcript forms encoding full-length and transcriptionally active p73 proteins, in addition to ΔN-p73. We also show that together with the acquired expression of TA-p73, the ‘retinoblastoma pathway’ is inactivated, and E2F1-target genes including cyclin E and p14ARF are activated in hepatocellular carcinoma. However, there was no full correlation between ‘retinoblastoma pathway’ inactivation and TA-p73 expression. Most TA-p73-expressing hepatocellular carcinoma cells have also lost p53 function either by lack of expression or missense mutations. The p73 gene, encoding only ΔN-p73 protein, may function as a tumour promoter rather than a tumour suppressor in liver tissue. This may be one reason why p73 is not a mutation target in hepatocellular carcinoma.
| Item Type: | Article |
|---|---|
| Schools: | Schools > School of Environment and Life Sciences |
| Journal or Publication Title: | Oncogene |
| Publisher: | Springer Nature |
| ISSN: | 0950-9232 |
| Depositing User: | BS Sayan |
| Date Deposited: | 06 Feb 2023 15:12 |
| Last Modified: | 06 Feb 2023 15:12 |
| URI: | https://usir.salford.ac.uk/id/eprint/66355 |
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