Journal
CANCER CELL
Volume 28, Issue 4, Pages 486-499Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2015.09.001
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Funding
- NCI Cancer Center [CA16672]
- NIH [P50 CA1000632-09]
- Leukemia Research Foundation
- Center for Genetics and Genomics
- MDACC
- Cancer Research Innovation Spain
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hnRNP K regulates cellular programs, and changes in its expression and mutational status have been implicated in neoplastic malignancies. To directly examine its role in tumorigenesis, we generated a mouse model harboring an Hnrnpk knockout allele (Hnrnpk(+/-)). Hnrnpk haploinsufficiency resulted in reduced survival, increased tumor formation, genomic instability, and the development of transplantable hematopoietic neoplasms with myeloproliferation. Reduced hnRNP K expression attenuated p21 activation, downregulated C/EBP levels, and activated STAT3 signaling. Additionally, analysis of samples from primary acute myeloid leukemia patients harboring a partial deletion of chromosome 9 revealed a significant decrease in HNRNPK expression. Together, these data implicate hnRNP K in the development of hematological disorders and suggest hnRNP K acts as a tumor suppressor.
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