STAT3 phosphorylation affects p53/p21 axis and KSHV lytic cycle activation

Roberta Santarelli, Valentina Carillo, Maria Anele Romeo, Aurelia Gaeta, Cristina Nazzari, Roberta Gonnella, Marisa Granato, Gabriella D'Orazi, Alberto Faggioni, Mara Cirone

Research output: Contribution to journalArticlepeer-review


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 languageEnglish
Pages (from-to)137-143
Number of pages7
Publication statusPublished - Feb 2019


  • KAP-1
  • KSHV
  • Lytic cycle
  • p21
  • p53
  • Ser727 STAT3
  • STAT3
  • Tyr705 STAT3

ASJC Scopus subject areas

  • Virology


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