Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

C-terminal truncated hepatitis B virus X protein regulates tumorigenicity, self-renewal and drug resistance via STAT3/Nanog signaling pathway.

Oncotarget - 4 Apr 2017

Ching Rachel Hiu Ha, Sze Karen Man Fong, Lau Eunice Yuen Ting, Chiu Yung-Tuen, Lee Joyce Man Fong, Ng Irene Oi Lin, Lee Terence Kin Wah

Abstract excerpt

Hepatitis B virus (HBV) is a major risk factor of chronic liver disease and hepatocellular carcinoma (HCC). Random integration of HBV DNA into the host genome is frequent in HCC leading to truncation of the HBV DNA, particularly at the C-terminal end of the HBV X protein (HBx). C-terminally truncated HBx (HBx-ΔC) has been implicated in playing a pro-oncogenic role in hepatocarcinogenesis. However, the mechanism...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cell Self Renewal
Share to Mice, Inbred NOD

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mice, SCID

Share to Nanog Homeobox Protein

Share to Neoplastic Stem Cells

Share to STAT3 Transcription Factor

Share to Transplantation, Heterologous

Share to Viral Regulatory and Accessory Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 28186991
DOI: 10.18632/oncotarget.15183
PMCID: PMC5410322

Genes

STAT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

C-terminal truncated hepatitis B virus X protein regulates tumorigenicity, self-renewal and drug resistance via STAT3/Nanog signaling pathway.PMID 28186991Read ↗

Cancer Stem Cell Functions in Hepatocellular Carcinoma and Comprehensive Therapeutic StrategiesSemantic proximity Read ↗

HBx Facilitates Drug Resistance in Hepatocellular Carcinoma via CD133-regulated Self-renewal of Liver Cancer Stem CellsSemantic proximity Read ↗

Turning Hepatic Cancer Stem Cells Inside Out – A Deeper Understanding through Multiple PerspectivesSemantic proximity Read ↗

Hepatitis B Viral Protein HBx and the Molecular Mechanisms Modulating the Hallmarks of Hepatocellular Carcinoma: A Comprehensive ReviewSemantic proximity Read ↗

The oncogenic role of hepatitis B virus X gene in hepatocarcinogenesis: recent updatesSemantic proximity Read ↗

C8orf4 negatively regulates self-renewal of liver cancer stem cells via suppression of NOTCH2 signallingSemantic proximity Read ↗

Molecular mechanism of hepatitis B virus X protein function in hepatocarcinogenesisSemantic proximity Read ↗

Hepatitis B virus-induced hepatocellular carcinoma.Semantic proximity Read ↗

The oncogenic potential of NANOG: An important cancer induction mediatorSemantic proximity Read ↗

Coexpression of gene Oct4 and Nanog initiates stem cell characteristics in hepatocellular carcinoma and promotes epithelial-mesenchymal transition through activation of Stat3/Snail signalingSemantic proximity Read ↗

Hepatitis B virus X protein-mediated non-coding RNA aberrations in the development of human hepatocellular carcinomaSemantic proximity Read ↗

BCL11B suppresses tumor progression and stem cell traits in hepatocellular carcinoma by restoring p53 signaling activitySemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.