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Cell growth inhibition by all-trans retinoic acid in SKBR-3 breast cancer cells: Involvement of protein kinase Cα and extracellular signal-regulated kinase mitogen-activated protein kinase

✍ Scribed by Shino Nakagawa; Teruhiko Fujii; Goro Yokoyama; Marcelo G. Kazanietz; Hideaki Yamana; Kazuo Shirouzu

Publisher
John Wiley and Sons
Year
2003
Tongue
English
Weight
359 KB
Volume
38
Category
Article
ISSN
0899-1987

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✦ Synopsis

Abstract

All‐trans retinoic acid (ATRA), a synthetic derivative of vitamin A, inhibits the growth of breast cancer cells. To elucidate the mechanism by which ATRA causes cell growth inhibition, we examined changes in cell cycle and intracellular signaling pathways, focusing on protein kinase C (PKC) and mitogen‐activated protein kinase (MAPK). Using the estrogen receptor‐negative, retinoid receptor–positive breast cancer cell line SKRB‐3, we found that treatment with ATRA significantly decreased the expression of PKCα, as well as reducing ERK MAPK phosphorylation. ATRA treatment leads to dephosphorylation of Rb, and consequently to G~1~ arrest. Marked changes in the expression of cyclins (particularly cyclins A and E) were observed in SKBR‐3 cells treated with ATRA. Using a series of pharmacological and molecular approaches, we found evidence that ATRA‐induced SKBR‐3 cell growth inhibition involves the deregulation of the PKCα‐MAPK pathway. These data suggest that retinoids interfered with signal transduction pathways that are crucial for cell cycle progression, and highlight the complexities of the biological effects of retinoid derivatives. © 2003 Wiley‐Liss, Inc.

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