Literature DB >> 23221504

Sphingosine induces apoptosis in MKN-28 human gastric cancer cells in an SDK-dependent manner.

Takeshi Kanno1, Takaaki Nishimoto, Yumiko Fujita, Akinobu Gotoh, Takashi Nakano, Tomoyuki Nishizaki.   

Abstract

BACKGROUND/AIMS: Evidence has pointed to the role of sphingosine in cellular differentiation, cell growth, and apoptosis. The present study investigated sphingosine-induced apoptosis in human gastric cancer cells.
METHODS: Well differentiated MKN-28 and poorly differentiated MKN-45 human gastric cancer cells were cultured. MTT assay, TUNEL staining, Western blotting, and assay of caspase-3, -8, and -9 activities were carried out in cells transfected with and without the siRNA to silence the protein kinase C (PKC)-δ-targeted gene.
RESULTS: Sphingosine induced apoptosis in MKN-28 cells, with the potential much greater than for MKN-45 cells. Transfection with the siRNA to silence the PKC-δ-targeted gene (PKC-δ siRNA) into MKN-28 cells significantly reduced presence of sphingosine-dependent protein kinase (SDK) in association with reduced PKC-δ expression. Sphingosine-induced apoptosis in MKN-28 cells was prevented by transfecting with the PKC-δ siRNA. Sphingosine promoted SDK production from PKC-δ and increased phosphorylated 14-3-3 protein for MKN-28 cells, but such effects were not found with MKN-45 cells. Moreover, sphingosine perturbed mitochondrial membrane potentials and activated caspase-3 and caspase-9 in MKN-28 cells, which were also inhibited by transfecting with the PKC-δ siRNA.
CONCLUSION: The results of the present study indicate that sphingosine induces apoptosis in well differentiated MKN-28 human gastric cancer cells by increasing SDK production from PKC-δ, to phosphorylate 14-3- 3 protein, thereby causing disruption of mitochondrial membrane potentials and activating caspase-9 followed by the effector caspase-3.
Copyright © 2012 S. Karger AG, Basel.

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Year:  2012        PMID: 23221504     DOI: 10.1159/000341475

Source DB:  PubMed          Journal:  Cell Physiol Biochem        ISSN: 1015-8987


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