Abstract
The Tyr705 STAT3 constitutive activation, besides promoting PEL cell survival, contributes to the maintenance of viral latency. We found indeed that its de-phosphorylation by AG490 induced KSHV lytic cycle. Moreover, Tyr705 STAT3 de-phosphorylation, mediated by the activation of tyrosine phosphatases, together with the increase of Ser727 STAT3 phosphorylation contributed to KSHV lytic cycle induction by TPA. We then observed that p53-p21 axis, essential for the induction of KSHV replication, was activated by the inhibition of Tyr705 and by the increase of Ser727 STAT3 phosphorylation. As a possible link between STAT3, p53-p21 and KSHV lytic cycle, we found that TPA and AG490 reduced the expression of KAP-1, promoting p53 stability, p21 transcription and KSHV lytic cycle activation in PEL cells.
Original language | English |
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Pages (from-to) | 137-143 |
Number of pages | 7 |
Journal | Virology |
Volume | 528 |
DOIs | |
Publication status | Published - Feb 2019 |
Keywords
- KAP-1
- KSHV
- Lytic cycle
- p21
- p53
- Ser727 STAT3
- STAT3
- Tyr705 STAT3
ASJC Scopus subject areas
- Virology