BMB Rep. 2016; 49(10): 566-571  
Enhancement of UV-induced nucleotide excision repair activity upon forskolin treatment is cell growth-dependent
Jeong-Min Lee, Jeong-Min Park & Tae-Hong Kang*
Department of Biological Science, Dong-A University, Busan 49315, Korea
Correspondence to: Tel: +82-51-200-7261; Fax: +82-51-200-7269; E-mail: thkang@dau.ac.kr
Received: June 13, 2016; Revised: July 19, 2016; Accepted: July 27, 2016; Published online: October 31, 2016.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

Abstract
Forskolin (FSK), an adenylyl cyclase activator, has recently been shown to enhance nucleotide excision repair (NER) upon UV exposure. However, our study revealed that this effect was detected in human skin epithelial ARPE19 cells only in growing cells, but not in non-cycling cells. When the cells were grown at low density (70% confluence), FSK was capable of stimulating cAMP responsive element binding (CREB) phosphorylation, a marker for FSK-stimulated PKA activation, and resulted in a significant increase of NER activity compared to control treatment. However, cells grown under 100% confluent conditions showed neither FSK-induced CREB phosphorylation nor the resulting NER enhancement. These findings indicate that cellular growth is critical for FSK-induced NER enhancement and suggest that cellular growth conditions should be considered as a variable while evaluating a reagent's pharmacotherapeutic efficacy.
Keywords: ATR, Cell growth, Forskolin, Nucleotide excision repair, Ultraviolet (UV)


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