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Cancer Cell. 2009 Aug 4;16(2):161-71. doi: 10.1016/j.ccr.2009.05.018.

Tumor suppression by phospholipase C-beta3 via SHP-1-mediated dephosphorylation of Stat5.

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  • 1Division of Cell Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037, USA.

Abstract

Given its catalytic activity to generate diacylglycerol and inositol 1,4,5-trisphosphate, phospholipase C (PLC) is implicated in promoting cell growth. However, we found that PLC-beta3-deficient mice develop myeloproliferative disease, lymphoma, and other tumors. The mutant mice have increased numbers of hematopoietic stem cells with increased proliferative, survival, and myeloid-differentiative abilities. These properties are dependent on Stat5 and can be antagonized by the protein phosphatase SHP-1. Stat5-dependent cooperative transformation by active c-Myc and PLC-beta3 deficiency was suggested in mouse lymphomas in PLC-beta3(-/-) and in Emicro-myc;PLC-beta3(+/-) mice and human Burkitt's lymphoma cells. The same mechanism for malignant transformation seems to be operative in other human lymphoid and myeloid malignancies. Thus, PLC-beta3 is likely a tumor suppressor.

PMID:
19647226
[PubMed - indexed for MEDLINE]
PMCID:
PMC2744338
Free PMC Article

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