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Della Porta et al. Hepatoma Res 2017;3:34-42 Hepatoma Research
DOI: 10.20517/2394-5079.2016.39
www.hrjournal.net
Original Article Open Access

Comparison of p53 and prohibitin

expression in the spectrum of hepatitis,

cirrhosis, and hepatocellular carcinoma

Lívia Maria Della Porta , Fernando Silva Ramalho , Carlos Augusto Oliveira , Deisy Mara Silva , Marlei Josiele
1
2
1
1
Augusto , Leandra Náira Zambelli Ramalho
1
1
1 Department of Pathology and Legal Medicine, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP 14049-900, Brazil.
2 Department of Food Engineering, School of Animal Science and Food Engineering, University of São Paulo, Ribeirão Preto, SP 14049-900, Brazil.
Correspondence to: Dr. Leandra Náira Zambelli Ramalho, Department of Pathology, Faculty of Medicine of Ribeirão Preto, University of São Paulo,
Ribeirão Preto, SP 14049-900, Brazil. E-mail: lramalho@fmrp.usp.br
How to cite this article: Della Porta LM, Ramalho FS, Oliveira CA, Silva DM, Augusto MJ, Ramalho LNZ. Comparison of p53 and prohibitin
expression in the spectrum of hepatitis, cirrhosis, and hepatocellular carcinoma. Hepatoma Res 2017;3:34-42.
ABSTRACT

Article history: Aim: To investigate the correlation of p53 and prohibitin (PHB) expression in the spectrum of
Received: 16-09-2016 hepatitis, cirrhosis, and human hepatocellular carcinoma (HCC). Methods: Hepatic biopsies from
Accepted: 13-12-2016 patients with HCC (n = 60), cirrhosis (CIR, n = 30), hepatitis C virus (HCV, n = 30), and normal livers
Published: 28-02-2017 (NL, n = 20) were examined for immunohistochemical expression of RelA/p65, tumor necrosis
factor receptor-1 (TNFR1), TNF-related apoptosis-inducing ligand (TRAIL), p53, and PHB. The
Key words: samples were also analysed by nuclear factor kappa B (NFκB) Southwestern histochemistry and
p53, a transferase-mediated dUTP-biotin nick-end labelling assay. Results: Expression of NFκB and
prohibitin, RelA/p65 was detected increasingly from NL to CIR, but had a diminished labelling in the HCC
nuclear factor kappa B, cases (P < 0.05). Expression levels of TNFR1 and TRAIL followed the same pattern (P < 0.05).
apoptosis, Apoptosis was increased in HCC, but was progressively reduced from CIR to NL (P < 0.05). p53
hepatocellular carcinoma and PHB nuclear expressions were amplified in cases of HCC, but diminished in NL, HCV, and
CIR (P < 0.05). Conclusion: These results suggest that in addition to well-understood sequences
of proinflammatory events such as TNF-induced NFκB activation and NFκB/TRAIL pathway-
mediated apoptosis, development of HCC is also influenced by regulation of p53 and PHB tumour
suppressor function. Additional studies are necessary to explain the contradictory mechanisms of
the tumour microenvironment observed in the sequence of HCV, CIR, and HCC.

INTRODUCTION pathways involved in hepatic cancer have been the
focus of numerous studies.
Hepatocellular carcinoma (HCC), the most frequent
primary hepatic cancer, is the third highest cause Activation of the transcriptional factor nuclear factor
[1]
of cancer-related death worldwide. Accumulation kappa B (NFκB), an important modulator of inflammatory
[3]
of genetic and epigenetic alterations results in the and cell survival responses, has been associated with
[4]
development of HCC. Therefore, the molecular hepatic carcinogenesis. NFκB may be activated in
[2]
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