| First Author | Xiao W | Year | 2009 |
| Journal | Cancer Cell | Volume | 16 |
| Issue | 2 | Pages | 161-71 |
| PubMed ID | 19647226 | Mgi Jnum | J:151972 |
| Mgi Id | MGI:4355642 | Doi | 10.1016/j.ccr.2009.05.018 |
| Citation | Xiao W, et al. (2009) Tumor suppression by phospholipase C-beta3 via SHP-1-mediated dephosphorylation of Stat5. Cancer Cell 16(2):161-71 |
| abstractText | 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. |
