Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
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
Doi: 10.1016/j.ejca.2017.06.003
Web of Science
PubMed
FullText
FullText_MUG
- Führende Autor*innen der Med Uni Graz
- Golob-Schwarzl Nicole
- Haybäck Johannes
- Co-Autor*innen der Med Uni Graz
- Birkl-Töglhofer Anna Maria
- Fickert Peter
- Gogg-Kamerer Margit
- Kraßnig Stefanie
- Schicho Rudolf
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- Abstract:
- 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