Stat3 activation of NF-κB p100 processing involves CBP/p300-mediated acetylation

Nagalakshmi Nadiminty, Wei Lou, Soo Ok Lee, Xin Lin, Donald L. Trump, Allen C Gao

Research output: Contribution to journalArticlepeer-review

110 Scopus citations


Activation of the noncanonical NF-κB signaling pathway involved in the proteolytic processing of NF-κB p100 to p52 is tightly regulated, and overproduction of p52 leads to lymphocyte hyperplasia and transformation. We have demonstrated that active but not latent Stat3, expressed in many types of human cancers involved in cell proliferation and survival, induces p100 processing to p52 by activation of IKKα and subsequent phosphorylation of p100. The Stat3-mediated p100 processing to p52 requires activation of Stat3 by the acetyltransferase activity of cAMP-response element-binding protein (CREB)-binding protein (CBP)/p300. A mutant of Stat3 defective in acetylation blocked Stat3-mediated p100 processing to p52 and acted as a dominant negative in blocking the production of p52. Furthermore, overexpression of p52 protected cells from apoptotic cell death. Thus, activation of the processing of p100 to p52 by Stat3 may represent one of the common pathways used by cancer cells to survive and escape therapy.

Original languageEnglish (US)
Pages (from-to)7264-7269
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number19
StatePublished - May 9 2006
Externally publishedYes


  • Apoptosis
  • Cancer
  • Cell signal
  • Prostate

ASJC Scopus subject areas

  • Genetics
  • General


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