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The insulin-like growth factor 2 (IGF2) mRNA-binding protein p62/IGF2BP2-2 as a promoter of NAFLD and HCC?
  1. Yvette Simon1,
  2. Sonja M Kessler1,2,
  3. Rainer M Bohle3,
  4. Johannes Haybaeck2,
  5. Alexandra K Kiemer1
  1. 1 Department of Pharmacy, Saarland University, Pharmaceutical Biology, Saarbrücken, Saarland, Germany
  2. 2 Institute of Pathology, Medical University of Graz, Graz, Austria
  3. 3 Department of Pathology, Saarland University, Homburg/Saar, Germany
  1. Correspondence to Prof. Alexandra K Kiemer, Department of Pharmacy, Saarland University, Pharmaceutical Biology, P.O. box 15 11 50, Saarbrücken 66041, Germany;{at}

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Non-alcoholic fatty liver disease (NAFLD) represents the most common hepatic manifestation of chronic liver diseases in developed countries. Since non-alcoholic steatohepatitis (NASH) is responsible for a large proportion of cryptogenic cirrhosis and cirrhosis represents the main risk factor for hepatocellular carcinoma (HCC), HCC is a severe complication of end-stage NAFLD.1

Recent evidence published in this journal showed the therapeutic potential of an inhibition of the chemokine (C-C motif) ligand 2 (CCL2)/monocyte chemoattractant protein-1 (MCP-1) in NASH.2 The study by Baeck et al elegantly demonstrated that the pharmacological administration of an RNA oligonucleotide against MCP-1 ameliorates murine steatosis and inflammation. Since mice deficient of the MCP-1 receptor also showed attenuated fibrosis, MCP-1 was suggested as a critical link in the axis steatosis–inflammation–fibrosis.2

Here, we report that animals with a liver-specific overexpression of the insulin-like growth factor 2 (IGF2) mRNA-binding protein p62/IMP2-2/IGF2BP2-2 exhibit distinctly elevated Ccl2 expression levels (figure 1A) when fed a methionine–choline-deficient (MCD) diet, which models all hepatic stages of NAFLD. Accordingly, in addition to elevated inflammatory gene expression, p62 transgenics had higher fat deposition (figure 1B) …

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