Open AccessTranslational Regulation in Hepatocellular Carcinogenesis
Author(s) -
Suzana Bracic Tomazic,
Christoph Schatz,
Johannes Haybaeck
Publication year - 2021
Publication title -
drug design, development and therapy
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.964
H-Index - 64
ISSN - 1177-8881
DOI - 10.2147/dddt.s255582
Subject(s) - hepatocellular carcinoma , carcinogenesis , pi3k/akt/mtor pathway , downregulation and upregulation , cirrhosis , cancer research , hepatitis b virus , medicine , signal transduction , hepatitis c virus , bioinformatics , biology , immunology , virus , cancer , genetics , gene
The mortality of hepatocellular carcinoma (HCC) is distributed unevenly worldwide. One of the major causes is hepatitis B or hepatitis C virus infection and the development and progression of liver cirrhosis. The carcinogenesis of HCC is among others regulated via the mTOR (mechanistic target of rapamycin) signaling pathway and represents a possible method of targeted treatment. The aim of our article was to address the most recent clinical advances and findings of basic studies on the mTOR signaling pathway and the involved factors. Risk factors play a key role in dysregulation of the signaling pathway, where both mTORCs are upregulated and protein synthesis is altered. eIFs and, to a lesser extent, eEFs play an essential role in this process. Whether the factor will be upregulated or downregulated, among others, depends on hepatitis B/C virus infection. The amount of a particular factor in a patient sample lets us know whether HCC recurrence will occur, what is the likelihood of chemoresistance, and what outcome is predicted for patients with an increased value. Our analysis shows that in addition to mTOR, eIF3, eIF4, and eIF5 play an important role, as they can serve as biomarkers for non- and virus-related HCC.