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Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid

Golob-Schwarzl, N; Krassnig, S; Toeglhofer, AM; Park, YN; Gogg-Kamerer, M; Vierlinger, K; Schröder, F; Rhee, H; Schicho, R; Fickert, P; Haybaeck, J.
New liver cancer biomarkers: PI3K/AKT/mTOR pathway members and eukaryotic translation initiation factors.
Eur J Cancer. 2017; 83(60):56-70
Web of Science PubMed FullText FullText_MUG


Autor/innen der Med Uni Graz:
Birkl-Töglhofer Anna Maria
Fickert Peter
Gogg-Kamerer Margit
Golob-Schwarzl Nicole
Haybäck Johannes
Kraßnig Stefanie
Schicho Rudolf

Dimensions Citations:

Plum Analytics:
Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related deaths worldwide. The initiation of protein translation is an important rate-limiting step in eukaryotes and is crucial in many viral infections. Eukaryotic translation initiation factors (eIFs) are involved in the initiation step of protein translation and are linked to the phosphatidylinositol-3-kinases PI3K/AKT/mTOR pathway. Therefore we aimed to investigate a potential role of eIFs in HCC. We herein report on the immunohistochemical expression of the various eIF subunits in 235 cases of virus-related human HCC. Additionally, we used immunoblot analysis to investigate the expression of virus-related HCC and non-virus-related HCC in comparison to controls. Mammalian target of rapamycin (or mechanistic target of rapamycin as it is known now (mTOR) and activated mTOR were significantly increased in chronic hepatitis C (HCV)-associated HCC, in HCC without a viral background, in alcoholic liver disease and Wilson disease. pPTEN, phosphatase and tensin homologue (PTEN) and pAKT showed a significant increase in HBV- and HCV-associated HCC, chronic hepatitis B, HCC without a viral background, alcoholic steatohepatitis (ASH) and Wilson disease. Phosphorylated (p)-eIF2α, eIF2α, eiF3B, eIF3D, eIF3J, p-eIF4B, eIF4G and eIF6 were upregulated in HCV-associated HCC. eIF2α, p-eIF4B, eIF5 and various eIF3 subunits were significantly increased in chronic hepatitis B (HBV)-associated HCC. HCC without viral background displayed a significant increase for the eIF subunits p-2α, 3C, 3I, 4E and 4G. We noticed engraved differences in the expression pattern between chronic hepatitis B and C, HBV- and HCV-associated HCC and non-virus-related HCC. Copyright © 2017 Elsevier Ltd. All rights reserved.
Find related publications in this database (using NLM MeSH Indexing)
Adult -
Aged -
Aged, 80 and over -
Biomarkers, Tumor - metabolism
Carcinoma, Hepatocellular - complications
Carcinoma, Hepatocellular - metabolism
Eukaryotic Initiation Factors - metabolism
Female -
Hepatitis B, Chronic - complications
Hepatitis B, Chronic - metabolism
Hepatitis C, Chronic - complications
Hepatitis C, Chronic - metabolism
Hepatolenticular Degeneration - complications
Hepatolenticular Degeneration - metabolism
Humans -
Immunohistochemistry -
Liver Diseases, Alcoholic - complications
Liver Diseases, Alcoholic - metabolism
Liver Neoplasms - complications
Liver Neoplasms - metabolism
Male -
Middle Aged -
Phosphatidylinositol 3-Kinases - metabolism
Protein Subunits - metabolism
Proto-Oncogene Proteins c-akt - metabolism
Retrospective Studies -
TOR Serine-Threonine Kinases - metabolism

Find related publications in this database (Keywords)
Non-virus-related hepatocellular carcinoma
Virus-related hepatocellular carcinoma
Chronic hepatitis B
Chronic hepatitis C
Translation initiation
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