Journal
CANCER CELL
Volume 4, Issue 5, Pages 349-360Publisher
CELL PRESS
DOI: 10.1016/S1535-6108(03)00268-X
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Funding
- NCI NIH HHS [CA77735] Funding Source: Medline
- NIDDK NIH HHS [5P30DK32520] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R56CA077735, R01CA077735] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK032520] Funding Source: NIH RePORTER
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Wnt5a is a member of the Wnt family of secreted glycoproteins that play essential organizing roles in development. Similar to other Wnt members, Wnt5a can upregulate cell proliferation and has been proposed to have oncogenic function. Here we report that Wnt5a signals through the noncanonical Wnt/Ca++ pathway to suppress cyclin D1 expression and negatively regulate B cell proliferation in a cell-autonomous manner. Wnt5a hemizygous mice develop myeloid leukemias and B cell lymphomas that are clonal in origin and display loss of Wnt5a function in tumor tissues. Furthermore, analysis of human primary leukemias reveals deletion of the WNT5A gene and/or loss of WNT5A expression in a majority of the patient samples. These results demonstrate that Wnt5a suppresses hematopoietic malignancies.
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