AI Article Synopsis
- Numerous tumor viruses, including HTLV-1, HCV, and HPV, are responsible for about 15% of human cancers.
- Despite differences in their oncoproteins, these viruses share common methods for promoting cancer characteristics in infected cells.
- The review highlights recent findings on how these viruses induce epigenetic changes, impacting gene expression and contributing to cancer development without altering DNA sequences.
Article Abstract
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.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8346956 | PMC |
| http://dx.doi.org/10.3390/ijms22158346 | DOI Listing |
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