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Editorial

. 2019 Jan 18;10(6):629-630.

doi: 10.18632/oncotarget.26602.

AEG-1 targeting for inhibiting inflammation: potential anti-HCC strategy

Saranya Chidambaranathan Reghupaty¹, Rachel Mendoza¹, Devanand Sarkar¹

Affiliations

Affiliation

¹ Department of Human and Molecular Genetics, Massey Cancer Center, VCU Institute of Molecular Medicine (VIMM), Virginia Commonwealth University, Richmond, VA, USA.

PMID: 30774759
PMCID: PMC6363015
DOI: 10.18632/oncotarget.26602

Editorial

AEG-1 targeting for inhibiting inflammation: potential anti-HCC strategy

Saranya Chidambaranathan Reghupaty et al. Oncotarget. 2019.

. 2019 Jan 18;10(6):629-630.

doi: 10.18632/oncotarget.26602.

Authors

Saranya Chidambaranathan Reghupaty¹, Rachel Mendoza¹, Devanand Sarkar¹

Affiliation

¹ Department of Human and Molecular Genetics, Massey Cancer Center, VCU Institute of Molecular Medicine (VIMM), Virginia Commonwealth University, Richmond, VA, USA.

PMID: 30774759
PMCID: PMC6363015
DOI: 10.18632/oncotarget.26602

No abstract available

Keywords: AEG-1; HCC; NF-kappaB; inflammation; macrophages.

PubMed Disclaimer

Figures

Figure 1. Cartoon showing the mechanism by which AEG-1 regulates the inflammatory process and HCC development
Left panel. In Wild-type (WT) mice injury to hepatocytes activates NF-κB and IL-1 production that activates NF-κB and IL-6 production in the macrophages. IL-6 activates oncogenic STAT3 in hepatocytes facilitating transformation and development of HCC. Right panel. In the absence of AEG-1 (AEG-1KO), NF-κB activation is inhibited in hepatocytes and macrophages, thereby abrogating the inflammatory signaling and HCC development. Adapted from Reference 2.

See this image and copyright information in PMC

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References

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