Epigenetic regulation of histone H3 in the process of hepatocellular tumorigenesis.
Dan LiZhenguo ZengPublished in: Bioscience reports (2019)
Better understanding of epigenetic regulation of hepatocellular carcinoma (HCC) will help us to cure this most common malignant liver cancer worldwide. The underlying mechanisms of HCC tumorigenesis are genomic aberrations regulated by genetic and epigenetic modifications. Histone H3 lysine modifications regulate histone structure and modulate transcriptional factor binding with target gene promoters. Targetting genes include VASH2, fatty acids synthase, RIZ1, FBP1, MPP1/3, YAP, which affect tumorigenesis, metabolisms, angiogenesis, and metastasis. Signal pathway studies demonstrate that the HGF-MET-MLL axis, phosphatase and tensin homolog (PTEN)-PI3K-Akt axis; WNT-β-catenin signal pathway is involved in histone H3 modification. A variety of factors such as virus infection, reactive oxygen species, food-borne toxins, irradiation, or non-coding RNA cause hepatocellular DNA damage or modification. Dysfunctional DNA repair mechanisms, including those at the epigenetic level are also major causes of HCC tumorigenesis. The development of therapies based on epigenetic regulatory mechanisms has great potential to advance the care of HCC patients in the future.
Keyphrases
- dna repair
- pi k akt
- dna damage
- dna methylation
- cell proliferation
- genome wide
- copy number
- gene expression
- signaling pathway
- reactive oxygen species
- fatty acid
- end stage renal disease
- cell cycle arrest
- newly diagnosed
- ejection fraction
- acute myeloid leukemia
- epithelial mesenchymal transition
- chronic kidney disease
- oxidative stress
- transcription factor
- dna damage response
- stem cells
- endothelial cells
- palliative care
- quality improvement
- human health
- vascular endothelial growth factor
- radiation therapy
- amino acid
- dna binding
- climate change
- patient reported