Journal
CELL CYCLE
Volume 15, Issue 12, Pages 1552-1557Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2016.1164372
Keywords
9q21; 32; acute myeloid leukemia; c-Myc; C; EBP; hnRNP K; haploinsufficiency; mouse models; p53; p21
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Funding
- NCI Cancer Center [CA16672]
- NIH Career Development Award [P50 CA1000632-09]
- Leukemia Research Foundation Award
- Center for Genetics and Genomics Award
- Ladies Leukemia League
- MDACC MDS/AML Moonshot
- MDACC start-up funds
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The classification of a gene as an oncogene or a tumor suppressor has been a staple of cancer biology for decades. However, as we delve deeper into the biology of these genes, this simple classification has become increasingly difficult for some. In the case of heterogeneous nuclear ribonuclear protein K (hnRNP K), its role as a tumor suppressor has recently been described in acute myeloid leukemia and demonstrated in a haploinsufficient mouse model. In contrast, data from other clinical correlation studies suggest that hnRNP K may be more fittingly described as an oncogene, due to its increased levels in a variety of malignancies. hnRNP K is a multifunctional protein that can regulate both oncogenic and tumor suppressive pathways through a bevy of chromatin-, DNA-, RNA-, and protein-mediated activates, suggesting its aberrant expression may have broad-reaching cellular impacts. In this review, we highlight our current understanding of hnRNP K, with particular emphasis on its apparently dichotomous roles in tumorigenesis.
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