| Literature DB >> 27049467 |
Miguel Gallardo1, Marisa J Hornbaker1,2, Xiaorui Zhang1, Peter Hu3, Carlos Bueso-Ramos4, Sean M Post1.
Abstract
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.Entities:
Keywords: 9q21.32; C/EBP; acute myeloid leukemia; c-Myc; haploinsufficiency; hnRNP K; mouse models; p21; p53
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Year: 2016 PMID: 27049467 PMCID: PMC4934053 DOI: 10.1080/15384101.2016.1164372
Source DB: PubMed Journal: Cell Cycle ISSN: 1551-4005 Impact factor: 4.534