Journal
FRONTIERS IN ONCOLOGY
Volume 9, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2019.01421
Keywords
hepatocellular carcinoma; cell death; inflammation; BCL-2 family; BH3; primed to death; BH3 profiling; mitochondrial apoptosis
Categories
Funding
- German Research Foundation [MA 4443/2-2, SFB1292]
- Volkswagen Foundation (Lichtenberg program)
- Wilhelm-Sander Foundation [2017.007.1]
- DFG Heisenberg program, the Collaborative Research Cluster (CRC) 746
- Else Kroner-Fresenius-Stiftung
- Wilhelm-Sander Foundation
- Germany's Excellence Strategy [CIBSS - EXC-2189, 390939984]
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Hepatocellular carcinoma (HCC) ranks among the most rapidly evolving cancers in the Western world. The majority of HCCs develop on the basis of a chronic inflammatory liver damage that predisposes liver cancer development and leads to deregulation of multiple cellular signaling pathways. The resulting dysbalance between uncontrolled proliferation and impaired predisposition to cell death with consecutive failure to clear inflammatory damage is a key driver of malignant transformation. Therefore, resistance to death signaling accompanied by metabolic changes as well as failed immunological clearance of damaged pre-neoplastic hepatocytes are considered hallmarks of hepatocarcinogenesis. Hereby, the underlying liver disease, the type of liver damage and individual predisposition to apoptosis determines the natural course of the disease as well as the therapeutic response. Here, we will review common and individual aspects of cell death pathways in hepatocarcinogenesis with a particular emphasis on regulatory networks and key molecular alterations. We will further delineate the potential of targeting cell death-related signaling as a viable therapeutic strategy to improve the outcome of HCC patients.
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