Epac inhibits migration and proliferation of human prostate carcinoma cells.

British Journal of Cancer
M GrandochA-A Weber

Abstract

It was recently found that cAMP mediates protein kinase A-independent effects through Epac proteins. The aim of this study was to investigate the role of Epac in migration and proliferation of prostate carcinoma cells. The effect of Epac activation was determined by [(3)H]thymidine incorporation and scratch assays in PC-3 and DU 145 cells. Furthermore, cytoskeletal integrity was analysed by phalloidin staining. The participation of intracellular Epac effectors such as mitogen-activated protein (MAP) kinases, Rap1- and Rho-GTPases was determined by immunoblotting and pull-down assay. The specific Epac activator 8-pCPT-2'-O-Me-cAMP (8-pCPT) interfered with cytoskeletal integrity, reduced DNA synthesis, and migration. Although 8-pCPT activated Rap1, it inhibited MAP kinase signalling and RhoA activation. These findings were translated into functional effects such as inhibition of mitogenesis, cytoskeletal integrity, and migration. In human prostate carcinoma cells, Epac inhibits proliferative and migratory responses likely because of inhibition of MAP kinase and RhoA signalling pathways. Therefore, Epac might represent an attractive therapeutic target in the treatment of prostate cancer.

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Citations

Jan 30, 2015·Frontiers in Oncology·Peder Rustøen BraadlandKristin Austlid Taskén
Nov 4, 2016·Scientific Reports·Faiza BaameurAnnemieke Kavelaars
Apr 15, 2014·Pigment Cell & Melanoma Research·Erdene BaljinnyamKousaku Iwatsubo
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Methods Mentioned

BETA
nucleotide exchange
flow cytometry
GTPase
pull-down

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