We also identified recurrent HBV integration events (in ≥ 4 HCCs) that were validated by RNA sequencing (RNA-seq) and Sanger sequencing at the known and putative cancer-related TERT, MLL4 and CCNE1 genes, which showed upregulated gene expression in tumor versus normal tissue.
We also identified recurrent HBV integration events (in ≥ 4 HCCs) that were validated by RNA sequencing (RNA-seq) and Sanger sequencing at the known and putative cancer-related TERT, MLL4 and CCNE1 genes, which showed upregulated gene expression in tumor versus normal tissue.
Upon pharmacological treatment with demethylating agent 5-aza-2'-deoxycytidine or histone deacetylase inhibitor trichostatin A, T-cadherin promoter hypermethylation and/or histone deacetylation was frequently observed in HCC samples and cell lines.
Total RNA was extracted from individual HCCs for assessment of mutations within exons 27, 28, 31, 33, and 34, and aberrant transcript of the M6p/Igf2r gene by reverse transcription (RT)-polymerase chain reaction (PCR)-single strand conformation polymorphism (SSCP) and RT-PCR analyses, respectively.
To provide a functional link between T-cadherin promoter methylation and T-cadherin growth regulation, we used the HepG2 hepatoma cell line that exhibits T-cadherin promoter methylation.
To address the role of IKK2-mediated NF-κB activation in hepatocytes in the pathogenesis of liver disease and HCC in Mdr2(-/-) mice, we generated Mdr2-deficient animals lacking IKK2 specifically in hepatocytes using the Cre-loxP system.
Thymoquinone inhibits cell proliferation through regulation of G1/S phase cell cycle transition in N-nitrosodiethylamine-induced experimental rat hepatocellular carcinoma.
These results indicate that individuals with mutant genotypes at EPHX and GSTM1 may be at greater risk of developing AFB1 adducts, p53 mutations, and HCC when exposed to AFB1.
These observations were further confirmed in vivo by the reciprocal control of TIS21 expression and FoxM1 phosphorylation in the diethylnitrosamine-induced HCCs and TIS21(-/-) mouse embryonic fibroblast (MEF), in addition to increased expression of cyclin B1 and cdk1 activity.
These identified proteins, which include stratifin (14-3-3), transgelin 2, heat-shock protein (HSP)70, HSP27, manganese superoxide dismutase, prohibitin, DJ1, α-enolase, peroxiredoxin 6, aldo-keto reductase family member B10, phosphoglycerate kinase 1, α-1-antitrypsin and nm23-H1, may play a role in the development of HCC.
These identified proteins, which include stratifin (14-3-3), transgelin 2, heat-shock protein (HSP)70, HSP27, manganese superoxide dismutase, prohibitin, DJ1, α-enolase, peroxiredoxin 6, aldo-keto reductase family member B10, phosphoglycerate kinase 1, α-1-antitrypsin and nm23-H1, may play a role in the development of HCC.