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Aberrant hnRNP K expression: All roads lead to cancer
Authors:Miguel Gallardo  Marisa J Hornbaker  Xiaorui Zhang  Peter Hu  Carlos Bueso-Ramos
Institution:1. Department of Leukemia, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA;2. The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX, USA;3. School of Health Professions, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA;4. Department of Hematopathology, The University of Texas, MD Anderson Cancer Center, Houston, TX, USA
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.
Keywords:9q21  32  acute myeloid leukemia  c-Myc  C/EBP  hnRNP K  haploinsufficiency  mouse models  p53  p21
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