Epigenetic aberrations in DNA methylation and HPTMs in hepatocellular carcinoma (HCC). (IMAGE)
Caption
(A) Global DNA hypomethylation contributes to genomic instability, while promoter hypermethylation leads to the silencing of tumour suppressor genes, promoting tumour progression. (B) HPTM writers, readers and erasers that are frequently overexpressed (red) or downregulated (blue) in HCC are depicted. Dysregulated expression of these epigenetic modulators disrupts histone modification patterns, leading to aberrant chromatin remodelling and altered accessibility. The resulting transcriptional reprogramming contributes to tumour growth, immune evasion, and therapy resistance. BRD, bromodomain-containing protein; CHD, chromodomain helicase DNA-binding protein; HAT, histone acetyltransferase; HDAC, histone deacetylase; HPTMs, histone post-translational modifications; KDM, lysine demethylase; KMT, lysine methyltransferase; MBD, methyl-CpG binding domain protein; Me, methylation; PRMT, protein arginine methyltransferase; SRA, SET and RING-associated domain-containing proteins; TSGs, tumour suppressor genes.
Credit
By Barbara Bueloni, Maite Garcia Fernandez de Barrena, Matias Antonio Avila, Juan Bayo, Guillermo Mazzolini
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Credit must be given to the creator. Only noncommercial uses of the work are permitted.
License
CC BY-NC