Kaposi's sarcoma-associated herpesvirus (KSHV) vIL-6 promotes cell proliferation and migration by upregulating DNMT1 via STAT3 activation.
basic_science · Level V
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- Record sourced from PubMed, PMID 24675762.
- Also identified by DOI 10.1371/journal.pone.0093478 and PMC identifier 3968168.
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Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV) is etiologically associated with Kaposi's sarcoma (KS), the most common AIDS-related malignancy. KSHV vIL-6 promotes KS development, but the exact mechanisms remain unclear. Here, we reported that KSHV vIL-6 enhanced the expression of DNA methyltransferase 1 (DNMT1) in endothelial cells,increased the global genomic DNA methylation, and promoted cell proliferation and migration. And this effect could be blocked by the DNA methyltransferase inhibitor, 5-azadeoxycytidine. We also showed that vIL-6 induced up-regulation of DNMT1 was dependent on STAT3 activation. Therefore, the present study suggests that vIL-6 plays a role in KS tumorigenesis partly by activating DNMT1 and inducing aberrant DNA methylation, and it might be a potential target for KS therapy.
Medical subject headings
- DNA (Cytosine-5-)-Methyltransferases
- Endothelial Cells
- Epigenesis, Genetic
- Herpesvirus 8, Human
- Interleukin-6
- STAT3 Transcription Factor
- Viral Proteins