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KMID : 1140120050100020111
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Cancer Prevention Research
2005 Volume.10 No. 2 p.111 ~ p.115
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Inhibition of Gap Junctional Intercellular Communication in TPA-treated Normal Human Breast Epithelial Cells
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Park Joon-Suk
Yang Se-Ran
Ahn Nam-Shik
Jung Ji-Won
Jo Eun-Hye
Hwang Jae-Woong
Park Jung-Ran
Lee Yong-Soon
Kang Kyung-Sun
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Abstract
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The phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), is a potent inhibitor of gap junctional intercellular communication (GJIC) in normal human breast basal epithelial cell (Type II HBECs). The induced inhibition of communication by TPA in Type II HBECs is associated with hyperphosphorylation of connexin 43, the connexin responsible for GJIC. Since the activation of p38 MAP kinases downregulate GJIC, we hypothesized that the inhibition of GJIC by TPA involved p38 MAP kinases. TPA treatment for 1 hour of Type II HBECs strongly did not activated extracellular signal regulated kinases (ERKs) but p38 MAP kinases, blocked gap junction by SL/DT assay, and induced connexin 43 hyperphosphorylation. These data suggest that p38 MAP kinase signaling pathway may be closely related functionally to the gap junction effects of the phorbol ester in human breast basal epithelial cells.
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KEYWORD
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Normal human breast epithelial cells, Gap junctional intercellular communication (GJIC), Connexin 43, 12-O-tetradecanoylphorbol-13-acetate (TPA), p38 MAP kinase
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