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

被引：24

作者：

Adiseshaiah, Pavan ^{[1
]}

Li, Jinfang ^{[1
]}

Vaz, Michelle ^{[1
]}

Kalvakolanu, Dhananjaya V. ^{[2
]}

Reddy, Sekhar P. ^{[1
]}

机构：

[1] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD 21205 USA

[2] Univ Maryland, Sch Med, Greenebaum Canc Ctr, Dept Microbiol & Immunol, Baltimore, MD 21201 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2008年 / 371卷 / 02期

关键词：

lung cancer cells; MAP kinases; ERK1/2; kinases; AP-1; c-jun;

D O I：

10.1016/j.bbrc.2008.04.063

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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. Published by Elsevier Inc.

引用

页码：304 / 308

页数：5

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