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PLoS One. 2014 Mar 27;9(3):e93478. doi: 10.1371/journal.pone.0093478. eCollection 2014.

Kaposi's sarcoma-associated herpesvirus (KSHV) vIL-6 promotes cell proliferation and migration by upregulating DNMT1 via STAT3 activation.

Author information

1
Department of Respiratory Medicine, Nanjing Chest Hospital, Nanjing, China.
2
Department of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
3
Department of Laboratory Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China; National Key Clinical Department of Laboratory Medicine, Nanjing, China.

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.

PMID:
24675762
PMCID:
PMC3968168
DOI:
10.1371/journal.pone.0093478
[Indexed for MEDLINE]
Free PMC Article
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