Role of Virus-Induced Host Cell Epigenetic Changes in Cancer.
Valeria PietropaoloCarla PreziosoValeria PietropaoloPublished in: International journal of molecular sciences (2021)
The tumor viruses human T-lymphotropic virus 1 (HTLV-1), hepatitis C virus (HCV), Merkel cell polyomavirus (MCPyV), high-risk human papillomaviruses (HR-HPVs), Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpes virus (KSHV) and hepatitis B virus (HBV) account for approximately 15% of all human cancers. Although the oncoproteins of these tumor viruses display no sequence similarity to one another, they use the same mechanisms to convey cancer hallmarks on the infected cell. Perturbed gene expression is one of the underlying mechanisms to induce cancer hallmarks. Epigenetic processes, including DNA methylation, histone modification and chromatin remodeling, microRNA, long noncoding RNA, and circular RNA affect gene expression without introducing changes in the DNA sequence. Increasing evidence demonstrates that oncoviruses cause epigenetic modifications, which play a pivotal role in carcinogenesis. In this review, recent advances in the role of host cell epigenetic changes in virus-induced cancers are summarized.
Keyphrases
- dna methylation
- gene expression
- hepatitis b virus
- epstein barr virus
- hepatitis c virus
- endothelial cells
- single cell
- cell therapy
- genome wide
- papillary thyroid
- long noncoding rna
- high glucose
- squamous cell
- stem cells
- mesenchymal stem cells
- transcription factor
- liver failure
- pluripotent stem cells
- diabetic rats
- young adults
- lymph node metastasis
- oxidative stress
- circulating tumor cells
- circulating tumor