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 7

Progression mechanisms for the pathogenesis of PBC&PSC and the hepatocarcinogenesis through PBC&PSC. The blue, red, green, and yellow lines represent the interactions (or regulations) in PBC&PSC pathogenesis, PBC&PSC hepatocarcinogenesis, the hepatocarcinogenesis of normal liver through PBC&PSC, and the aggressive tumor progression, respectively, based on Figures 3 and 4. The epigenetic modifications of HIST2H2BE and RPL23A could facilitate the dysfunction of autoimmune-related progression through dysregulations of the WNT and the MAPK signaling pathways resulting in PBC&PSC. The accumulated epigenetic modifications and the dysregulation of miR-29a, miR-122, and miR-21 could facilitate the dysfunction of metabolism-related, apoptosis-related, autoimmune-related and DNA repair-related progression through the dysregulation of the WNT and the MAPK signaling pathways resulting in HCC. Dysregulation of miR-21, miR-122, and miR-29a could contribute to tumor invasion and metastasis to facilitate further aggressive tumor progression.