Investigating Pathogenic and Hepatocarcinogenic Mechanisms from Normal Liver to HCC by Constructing Genetic and Epigenetic Networks via Big Genetic and Epigenetic Data Mining and Genome-Wide NGS Data Identification

Figure 6

Progression mechanisms for the pathogenesis of NAFLD&NASH and the hepatocarcinogenesis through NAFLD&NASH. The blue, red, green, and yellow lines represent the interactions (or regulations) in NAFLD&NASH pathogenesis, NAFLD&NASH hepatocarcinogenesis, the hepatocarcinogenesis of normal liver through NAFLD&NASH, and the aggressive tumor progression, respectively, based on Figures 5 and 2. The epigenetic modification of HIST2H2BE could facilitate the dysfunction of metabolism-related progression through the dysregulations of the WNT and the MAPK signaling pathways resulting in NAFLD&NASH. The accumulated epigenetic modifications and dysregulations of miR-21 could facilitate the dysfunctions of metabolism-related, apoptosis-related, and DNA repair-related progression through dysregulations of the WNT and the MAPK signaling pathways resulting in HCC. Dysregulation of miR-21 and miR-122 could contribute to tumor invasion and metastasis to facilitate further aggressive tumor progression.