The relationship between the expression of APE1 and P53 protein and overall survival time of patients with hepatocellular carcinoma has not been found.
In this study, we examined mRNA expression by quantitative real-time PCR (qRT-PCR) of HOXA10 as well as histone deacetylase (HDAC) and protein levels by Western blot of HOXA10, HDAC1, Cyclin D1, proliferating cell nuclear antigen (PCNA), Survivin and p53 acetylation in HCC tissues and cell lines.
To clarify whether the level of p53 expression determines the apoptotic response of hepatocellular carcinoma (HCC) cells, we assessed the effect of various levels of expression of p53 gene on a p53-deficient HCC cell line, Hep3B, utilizing a doxycycline (Dox)-regulated inducible p53 expression system.
Immunostaining with monoclonal pAb 1801 revealed expression of p53 protein in tumor-cell nuclei in one HCV-associated HCC, and in no case of HBV-associated HCC, while the nuclei of adjacent hepatocytes were negative.
In the 132 matched HCC tissues, high expression levels of CDC20 were detected in 68.18% HCC samples, and overexpression of CDC20 was positively correlated with gender (P=0.013), tumor differentiation (P=0.000), TNM stage (P=0.012), P53 and Ki-67 expression (P=0.023 and P=0.007, respectively).
Analysis of transforming growth factor (TGF)-alpha/epidermal growth factor receptor, hepatocyte growth Factor/c-met,TGF-beta receptor type II, and p53 expression in human hepatocellular carcinomas.
miR-1228 functions as an oncogene by promoting cell cycle progression and cell mobility and negatively regulates the expression of p53. p53 downregulation in turn leads to an increase in miR-1228 expression, thereby forming a positive feedback loop that contributes to cancerogenesis in HCC.
MicroRNA-206 prevents the pathogenesis of hepatocellular carcinoma by modulating expression of met proto-oncogene and cyclin-dependent kinase 6 in mice.
In this study, we examined PICT1 expression levels and the status of TP53 in 51 primary HCC tissues in order to determine the clinical significance of PICT1 expression and the function of PICT1 in HCC cells.
In this study, we found that overexpression of ICN, the constitutive activated form of Notch1, up-regulated p53 protein expression in HCC cells by inhibiting proteasome degradation. p53 up-regulation was further observed in human primary hepatocellular carcinoma cells after activation of Notch signaling.
Treatment of primary cancer cells from patients with HCC expressing both phospho-FGFR and phospho-MET with PHA665752 did not induce cell death, whereas AZD4547 treatment induced cell death through the cleavage of caspase-3.
Finally, p53 (22,23) expressed from large plasmid quantity (1 microg) is crippled for the mediation of apoptosis in p53-negative Hep3B hepatocarcinoma cells.
The expression in HA was variable and differed between molecular subtypes of this neoplasm: inflammatory and HNF1A mutation-associated type are characterized by overexpression of c-MET to an extent comparable with poorly-differentiated HCC, whereas Wnt/β-catenin dysfunction-associated type lacks overexpression, and the amount of c-MET protein accumulated in its cells is similar to the levels in non-neoplastic tissue and well- to moderately-differentiated HCC.
Colony formation was reduced dramatically in those HCC cell lines in which ZBP-89 overexpression was demonstrated; this appeared to correlate with increased apoptosis, inferred by finding elevated levels of cleaved poly(ADP-ribose)polymerases (PARP), the probable mechanisms for which may involve increased p53 or p21 expression.
However, the mechanism by which p53 transcription regulation is modulated by hepatitis B virus X protein (HBx), a transcription cofactor implicated in hepatitis B virus-associated hepatocellular carcinoma (HCC), is poorly understood.