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Oncotarget. 2016 Jul 28;8(34):56095-56109. doi: 10.18632/oncotarget.10893. eCollection 2017 Aug 22.

Hepatic B cell leukemia-3 suppresses chemically-induced hepatocarcinogenesis in mice through altered MAPK and NF-κB activation.

Oncotarget

Nadine Gehrke, Marcus A Wörns, Amrit Mann, Yvonne Huber, Nadine Hoevelmeyer, Thomas Longerich, Ari Waisman, Peter R Galle, Jörn M Schattenberg

Affiliations

  1. Department of Medicine and University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
  2. Institute for Molecular Medicine, University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
  3. Institute of Pathology, University Hospital RWTH Aachen, Aachen, Germany.

PMID: 28915576 PMCID: PMC5593547 DOI: 10.18632/oncotarget.10893

Abstract

The transcriptional nuclear factor kappa B (NF-κB)-coactivator B cell leukemia-3 (Bcl-3) is a molecular regulator of cell death and proliferation. Bcl-3 has been shown to be widely expressed in different cancer types including hepatocellular carcinoma (HCC). Its influence on hepatocarcinogenesis is still undetermined. To examine the role of Bcl-3 in hepatocarcinogenesis mice with hepatocyte-specific overexpression of Bcl-3 (Bcl-3

Keywords: B cell leukemia-3 (Bcl-3); apoptosis; hepatocellular carcinoma (HCC); mitogen-activated protein kinase (MAPK); nuclear factor kappa B (NF-kB)

Conflict of interest statement

CONFLICTS OF INTERESTS All authors declare no conflicting interests.

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