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Carcinogenesis Advance Access published online on September 12, 2008
Carcinogenesis, doi:10.1093/carcin/bgn213
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© The Author 2008. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Organochlorine mediated potentiation of the general coactivator p300 through p38 mitogen-activated protein kinase *

Melyssa R. Bratton§§,¶,{Delta}, Daniel E. Frigo{ddagger},§,¶,{Delta}, Katinka A. Vigh, Daju Fan||, Scott Wadsworth¤, John A. McLachlan,§§ and Matthew E. Burow,**,{ddagger}{ddagger},¥

§ Molecular and Cellular Biology Program
Center for Bioenvironmental Research
** Department of Medicine-Section of Hematology and Medical Oncology
{ddagger}{ddagger} Department of Surgery
§§ Department of Pharmacology, Tulane University Health Science Center, New Orleans, LA 70112
|| Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina 27710
¤ Johnson & Johnson Pharmaceutical Research & Development, Raritan, NJ 08869-0602
{ddagger}

¥ To whom correspondence should be addressed: Matthew E. Burow, Department of Medicine, Division of Hematology/Oncology, Tulane University Health Sciences Center, 1430 Tulane Ave. SL-78, New Orleans, LA 70112, phone: (504)988-6688; Fax: (504)988-6215; email: mburow{at}tulane.edu

The activity of nuclear transcription factors is often regulated by specific kinase signaling pathways. We have previously shown the organochlorine pesticide DDT [dichlorodiphenyltrichloroethane] stimulates AP-1 [activator protein-1] activity through the p38 MAPK [mitogen-activated protein kinase]. Here, we show DDT and its metabolites also stimulate the transcriptional activity of CREB [cAMP response element binding protein] and Elk1 and potentiate gene expression through cAMP and hypoxia response elements. Because DDT stimulates gene expression through various transcription factors and hence, multiple response elements, we hypothesized p38 signaling targets a common shared transcriptional activator. Here, we demonstrate using both pharmacological and molecular techniques, the general coactivator p300 is phosphorylated and potentiated by the p38 MAPK signaling cascade. We further show that p38 directly phosphorylates p300 in its N-terminus. These results, together with our previous work, suggest that p38 stimulates downstream transcription factors in part by targeting the general coactivator p300.

{Delta} These two authors contributed equally to this manuscript and should both be considered first authors.

Received July 21, 2008; revised August 28, 2008; accepted September 1, 2008.


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