Paper Information

Title: 

CYCLIC AMP AS CHEMORESISTANCE FACTOR TO TOPOISOMERASE II INHIBITOR, DOXORUBICIN, FOR HUMAN PRE-B NALM-6 CELLS: A MECHANISM INVOLVED P53 DOWN-REGULATION AND NF-KAPPA B ACTIVATION

Type: SPEECH
Author(s): ZAND H.*,SAFA MAJID
 
 *NATIONAL NUTRITION AND FOOD TECHNOLOGY RESEARCH INSTITUTE, FACULTY OF NUTRITION SCIENCE AND FOOD TECHNOLOGY, SHAHID BEHESHTI UNIVERSITY, TEHRAN, IRAN
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2009Volume 19
 
 
Abstract: 

The cAMP has been implicated to exert regulative effect on proliferation and apoptosis in a variety of cells. Activation cAMP/ PKA pathway regulates reversible phosphorylation of several proteins that involved in cell cycle and apoptosis. Since DNA damage signaling consists of several proteins that potentially can be target of PKA/ cAMP, therefore, we speculated that cAMP/PKA may cross- talk with DNA damage signaling. In the current study we addressed the inhibitory effect of cAMP in doxorubicin induced apoptosis in pre-B Nalm-6 cells. We found that cAMP activators interfered with DNA damage through p53 dephosphorylation at Ser15 and decrease p53 accumulation. Moreover, elevation of cAMP potentiated IkB phosphorylation and DNA biding of NF-kB induced by DNA damage in spite of early inhibition of NF-kB. Taken together, our results demonstrated that cAMP impairs the balance between apoptotic and antiapoptotic transcription factors which their activation are hallmarks of DNA damage signaling.

 
Keyword(s): DOXORUBICIN, DNA DAMAGE, P53, IΚB, NF-ΚB, PP2A
 
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