Role of p63 and p73 isoforms on the cell death in patients with hepatocellular carcinoma submitted to orthotopic liver transplantation

Male 0301 basic medicine Hepatitis B virus Carcinoma, Hepatocellular Science 610 Neoplasias hepáticas 03 medical and health sciences Cell Line, Tumor Humans Protein Isoforms Carcinoma, Hepatocellular; Cell Death; Cell Line, Tumor; Female; Gene Expression Regulation, Neoplastic; Hepatitis B; Hepatitis B virus; Humans; Liver; Liver Neoplasms; Male; Protein Isoforms; Receptors, Death Domain; Transcription Factors; Tumor Protein p73; Tumor Suppressor Proteins; Liver Transplantation Línea celular tumoral Virus de la Hepatitis B Regulación neoplásica de la expresión génica Hígado Cell Death Trasplante de hígado Tumor Suppressor Proteins Q Liver Neoplasms R Tumor Protein p73 Receptors, Death Domain Hepatitis B Muerte celular Liver Transplantation 3. Good health Gene Expression Regulation, Neoplastic Liver Medicine Female Carcinoma hepatocelular Research Article Transcription Factors
DOI: 10.1371/journal.pone.0174326 Publication Date: 2017-03-28T19:18:24Z
ABSTRACT
Patients with hepatocellular carcinoma (HCC) submitted to orthotopic liver transplantation (OLT) have a variable 5-year survival rate limited mostly by tumor recurrence. The etiology, age, sex, alcohol, Child-Pugh, and the immunesuppressor been associated tumour expression of ΔNp73 is related reduced patients HCC. study evaluated p63 p73 isoforms cell death receptors, their relation recurrence survival. results were in vitro validated HCC lines.HCC sections from OLT used. was done differentiated hepatitis B virus (HBV)-expressing Hep3B control HepG2 cells. receptors cFLIPS/L, caspase-8 -3 activities, proliferation determined overexpressing cells.The TAp63 TAp73, increased ΔNp63 demonstrated that HBV-expressing vs cells showed p73, caspase activation, cFLIPL/cFLIPS ratio. overexpression TAp73 exerted more potent pro-apoptotic anti-proliferative effects than HepG2-transfected which cFLIPL upregulation.The reduction isoforms, rather alteration ΔN isoform expression, significant functional repercussion on HepB
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