443 HBX-Induced Repression of Mir224 Expression Relieves the Direct Inhibitory Effects of Mir224 on HBV Pgrna to Potentiate HBV Replication

Guerrieri, F.; Scisciani, C.; Belloni, Laura; Sbardellati, Andrea; Tramontano, Anna; Levrero, Massimo; Pediconi, Natalia

doi:10.1016/s0168-8278(12)60456-5

Cited by 1 publication

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…38 ChIPSeq genome-wide analysis of HBx chromatin recruitment revealed a specific binding of HBx to a large number of new and known HBx target sequences. 39 Systematic integrative analysis of the over 6,000 genes potentially regulated by HBx shows an enrichment in genes involved in cell metabolism, cell signaling, chromatin dynamics, and cancer but HBV replication (Ras, calcium transport, endocytosis, MAPK/WNT pathways, Src, the EGF/HGF family) as well. 37 HBx also binds to 115 miRNAs (70 putative miRNA promoters and 45 mirtrons), including mir224, mir21, and other miRNA deregulated in cancer, miRNA that control other cellular functions (i.e., miR26b, miR-502) and miRNAs that affect HBV replication (miR224, miR138, miR596, and others).…”

Section: The Hbx Proteinmentioning

confidence: 99%

See 1 more Smart Citation

Molecular Mechanisms of HBV-Associated Hepatocarcinogenesis

et al. 2013

View full text Add to dashboard Cite

Hepatitis B virus (HBV) contributes to hepatocellular carcinoma (HCC) development through direct and indirect mechanisms. HBV-DNA integration into the host genome occurs at early steps of clonal tumor expansion and induces both genomic instability and direct insertional mutagenesis of diverse cancer-related genes. Prolonged expression of the viral regulatory protein HBx and the large envelope protein deregulate the cellular transcription program and proliferation control and sensitize liver cells to carcinogenic factors. Epigenetic changes targeting the expression of tumor suppressor genes occur early in the development of HCC. A major role is played by HBx that is recruited on cellular chromatin and modulates chromatin dynamics at specific gene loci. Compared with tumors associated with other risk factors, HBV-related tumors have a higher rate of chromosomal alterations and p53 inactivation by mutations, overexpress fetal liver/hepatic progenitor cells genes, and show a specific activation of the AKT pathway. The wnt/β-catenin pathway is also often activated, but HBV-related tumors display a low rate of activating β-catenin mutations. All available evidence strongly supports the notion that chronic HBV infection triggers both common and etiology-specific oncogenic pathways, thus playing a direct role beyond stimulation of host immune responses and chronic necroinflammatory liver disease.

show abstract

Section: The Hbx Proteinmentioning

confidence: 99%

“…40 Multiple transcription factors mediate the recruitment of HBx on the target chromatin (i.e., E2F1, CREB, β-catenin, NFkB). 39,40…”

Section: The Hbx Proteinmentioning

confidence: 99%