| Literature DB >> 19647226 |
Wenbin Xiao1, Hong Hong, Yuko Kawakami, Yuko Kato, Dianqing Wu, Hiroki Yasudo, Akiko Kimura, Hiromi Kubagawa, Luigi F Bertoli, Randall S Davis, Luan A Chau, Joaquin Madrenas, Cyrus C Hsia, Anargyros Xenocostas, Thomas J Kipps, Lothar Hennighausen, Atsushi Iwama, Hiromitsu Nakauchi, Toshiaki Kawakami.
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.Entities:
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Year: 2009 PMID： 19647226 PMCID： PMC2744338 DOI： 10.1016/j.ccr.2009.05.018
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743