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KMID : 0359320060460020097
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Korean Journal of Veterinary Research
2006 Volume.46 No. 2 p.97 ~ p.105
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The roles of PKC-δ on the regulation of insulin-Like growth factor(IGF)-I and insulin-Like growth factor binding protein-3 secretion by all-trans retinoic acid in MCF-7 cell
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이선미
김상훈/최광수/강창원
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Abstract
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All-trans retinoic acid (AtRA) induces growth inhibition and apoptosis in a variety of tumer cells, including MCF-7 cells. Insulin-like growth factors (IGFs) system has been reported to be associated with the development of cancer. Although MCF-7 cell with AtRA is to be the major stimulus for the cell growth and apoptosis, the mechanism of insulin-like growth factor-I (IGF-I)/insulin-like growth factor binding protein-3 (IGFBP-3) system remains to be elucidated. Thus, this study was conducted to the effect of AtRA on the gene expression and level of IGF-I and IGFBP-3. In addition, we investigated the involvement of PKC-${delta}$ on the IGF-I and IGFBP-3 secretion in MCF-7 cell. AtRA(${geq}10^{-7}M$) decreased the IGF-1 secretion and mRNA expressions, but increased IGFBP-3 secretion and mRNA expressions in MCF-7 cells. Especially, the treatment of AtRA at 72 hours caused a significant reduction in the IGF-I secretion and mRNA expressions but increment in IGFBP-3 secretion and mRNA expressions (p < 0.05). $10^{-7}M$ AtRA activated PKC-${delta}$ that is one among PKC-$iota$, ${alpha}$, ${lambda}$ and ${delta}$ in MCF-7 cell. Rotllerin, a PKC-${delta}$ inhibitor, blocked AtRA-induced inhibition of the IGF-I and mRNA expressions, and increase of lGFBP-3 and mRNA expressions in MCF-7 cell. Together, AtRA inhibited the IGF-I secretion and mRNA expressions, but increased IGFBP-3 secretion and mRNA expressions in MCF-7 cell. Furthermore, AtRA-induced alteration of IGF-I, IGFBP-3 secretion, and the gene expressions were mediated via PKC-${delta}$ activity.
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KEYWORD
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AtRA, IGF-I, MCF-7, IGFBP-3, PKC-δ
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