Cross-talks between c-Kit and PKC isoforms in HMC-1(560) and HMC-1(560,816) cells. Different role of PKCδ in each cellular line

The c-kit inhibitor STI571 represents one of the most important treatments for patients with mastocytosis. However, intracellular pathways modulated by this compound are not completely defined. Here, STI571 effect on Protein Kinase C (PKC) regulation is determined in HMC-1 mast cell lines. STI571 ac...

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Veröffentlicht in:	Cellular immunology 2015-02, Vol.293 (2), p.104-112
Hauptverfasser:	Tobío, Araceli, Alfonso, Amparo, Botana, Luis M
Format:	Artikel
Sprache:	eng
Schlagworte:	Apoptosis - drug effects Apoptosis - immunology Benzamides - pharmacology Blotting, Western Cell Line Enzyme Activation - immunology Flow Cytometry Humans Imatinib Mesylate Isoenzymes Mast Cells - immunology Piperazines - pharmacology Protein Kinase C - analysis Protein Kinase C - immunology Protein Kinase Inhibitors - pharmacology Proto-Oncogene Proteins c-kit - immunology Pyrimidines - pharmacology Signal Transduction - immunology
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Zusammenfassung:	The c-kit inhibitor STI571 represents one of the most important treatments for patients with mastocytosis. However, intracellular pathways modulated by this compound are not completely defined. Here, STI571 effect on Protein Kinase C (PKC) regulation is determined in HMC-1 mast cell lines. STI571 activates PKCδ isoform resulting in HMC-1(560) apoptosis. The apoptosis observed is PKCδ-dependent, since PKCδ-silencing avoids STI571 effect. c-kit inhibition implies nuclear PKCδ translocation characterized by a clear dependence on actin cytoskeleton integrity in HMC-1(560) cell line, but not in HMC-1(560,816). Therefore, PKCδ modulations can lead to a serious decrease in STI571 treatment-effectiveness.
ISSN:	1090-2163
DOI:	10.1016/j.cellimm.2014.12.004