Interplay of Genetic and Epigenetic Alterations in Hepatocellular Carcinoma

Abstract

Genetic and epigenetic alterations play prominent roles in hepatocarcinogenesis and their appearance varies depending on etiological factors, race and tumor progression. Intriguingly, distinct patterns of these genetic and epigenetic mutations are coupled not only to affect each other, but to trigger different types of tumorigenesis. The patterns and frequencies of somatic variations vary depending on the nature of the surrounding chromatin. On the other hand, epigenetic alterations often induce genomic instability prone to mutation. Therefore, genetic mutations and epigenetic alterations in hepatocellular carcinoma appear to be inseparable factors that accelerate tumorigenesis synergistically. We have summarized recent findings on genetic and epigenetic modifications, their influences on each other’s alterations and putative roles in liver tumorigenesis.

Keywords::

• DNA methylation
• epigenetic modifications
• genetic mutations
• hepatocellular carcinoma
• signaling pathways

Financial & competing interest disclosure

This research was supported by the Global Research Laboratory Program of the National Research Foundation (NRF) funded by the Ministry of Science, ICT and Future Planning (grant number NRF-2007-00013) and Collaborative Genome Program for Fostering New Post-Genome industry through the National Research Foundation of Korea (NRF) funded by the Ministry of Science ICT and Future Planning (grant number 2015M3C9A4053251) to Y-J Kim and by the Mid-Career Researcher Program (NRF-2012R1A2A2A01010176) funded by the Ministry of Science, ICT and Future Planning to J Kim-Ha. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

This research was supported by the Global Research Laboratory Program of the National Research Foundation (NRF) funded by the Ministry of Science, ICT and Future Planning (grant number NRF-2007-00013) and Collaborative Genome Program for Fostering New Post-Genome industry through the National Research Foundation of Korea (NRF) funded by the Ministry of Science ICT and Future Planning (grant number 2015M3C9A4053251) to Y-J Kim and by the Mid-Career Researcher Program (NRF-2012R1A2A2A01010176) funded by the Ministry of Science, ICT and Future Planning to J Kim-Ha. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.