ERK signaling regulates tumor promoter induced c-Jun recruitment at the Fra-1 promoter

Pavan Adiseshaiah, Jinfang Li, Michelle Vaz, Dhananjaya V. Kalvakolanu, Sekhar P. Reddy

Research output: Contribution to journalArticlepeer-review


Fra-1 as an integral part of AP-1 (Jun/Fos) drives transcriptional programs involved in several physiologic and pathologic processes. It is also critical for tumor cell motility and metastasis. We have previously shown that two critical elements of Fra-1 promoter, the upstream TPA response element (TRE) and the serum response element (SRE), are necessary for its induction in response to phorbol esters in human pulmonary epithelial cell lines. Here, we have investigated the roles of various MAP kinases in regulating Fra-1 expression in response to TPA. Using pharmacologic and genetic tools, we demonstrate a prominent role for ERK1/2, but not JNK1/2 and p38, signaling in the TPA-induced activation of specific transcription factors that bind to the AP1 site and the SRE. Inhibition of ERK1/2 pathway suppresses Elk1 activation, and c-Jun and Fra-2 recruitment to the promoter.

Original languageEnglish (US)
Pages (from-to)304-308
Number of pages5
JournalBiochemical and Biophysical Research Communications
Issue number2
StatePublished - Jun 27 2008


  • AP-1
  • ERK1/2 kinases
  • Lung cancer cells
  • MAP kinases
  • c-Jun

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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