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8316009 
Journal Article 
PKCdelta and MAPK mediate G(1) arrest induced by PMA in SKBR-3 breast cancer cells 
Yokoyama, G; Fujii, T; Tayama, K; Yamana, H; Kuwano, M; Shirouzu, K; , 
2005 
Yes 
Biochemical and Biophysical Research Communications
ISSN: 0006-291X
EISSN: 1090-2104 
ACADEMIC PRESS INC ELSEVIER SCIENCE 
SAN DIEGO 
720-726 
English 
15649406 
WOS:000226674800014 
The effects of activating endogenous protein kinase C (PKC) on cell proliferation and the cell cycle were investigated by treating the breast cancer cell line SKBR-3 with phorbol 12-myristate 13 acetate (PMA). This inhibited cell growth in a concentration-dependent manner, causing a marked arrest of cells in G(1). Pre-treatment with GF109203X completely blocked the antiproliferative effect of PMA, and pre-treatment with the PKCdelta inhibitor rottlerin partially blocked it. Infecting SKBR-3 cells with an adenovirus vector containing wild-type PKCdelta, WTPKCdeltaAdV, had similar effects on PMA. Infecting the cells with a dominant-negative PKCdeltaAdV construct blocked the growth inhibition induced by PMA. Downstream of PKC, PMA treatment inhibited extracellular signal-regulated kinase mitogen-activated protein kinase phosphorylation, up-regulated c-jun NH(2)-terminal kinase phosphorylation, and inhibited retinoblastoma (Rb) phosphorylation. These results strongly implicated PKC (mainly PKCdelta) in the G(1) arrest induced by PMA and suggested PKC as a target for breast cancer treatment.