Aberrant hnRNP K expression: All roads lead to cancer

Cell Cycle. 2016 Jun 17;15(12):1552-7. doi: 10.1080/15384101.2016.1164372.

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; C/EBP; acute myeloid leukemia; c-Myc; haploinsufficiency; hnRNP K; mouse models; p21; p53.

Publication types

  • Review

MeSH terms

  • Animals
  • CCAAT-Enhancer-Binding Proteins / genetics
  • CCAAT-Enhancer-Binding Proteins / metabolism
  • Carcinogenesis / genetics*
  • Carcinogenesis / metabolism
  • Carcinogenesis / pathology
  • Cyclin-Dependent Kinase Inhibitor p21 / genetics
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism
  • Disease Models, Animal
  • Gene Expression Regulation, Neoplastic*
  • Haploinsufficiency
  • Heterogeneous-Nuclear Ribonucleoprotein K / genetics*
  • Heterogeneous-Nuclear Ribonucleoprotein K / metabolism
  • Humans
  • Leukemia, Myeloid, Acute / genetics*
  • Leukemia, Myeloid, Acute / metabolism
  • Leukemia, Myeloid, Acute / pathology
  • Mice
  • Oncogene Proteins / genetics*
  • Oncogene Proteins / metabolism
  • Protein Binding
  • Proto-Oncogene Proteins c-myc / genetics
  • Proto-Oncogene Proteins c-myc / metabolism
  • Signal Transduction
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism
  • Tumor Suppressor Proteins / genetics*
  • Tumor Suppressor Proteins / metabolism

Substances

  • CCAAT-Enhancer-Binding Proteins
  • Cyclin-Dependent Kinase Inhibitor p21
  • Heterogeneous-Nuclear Ribonucleoprotein K
  • Oncogene Proteins
  • Proto-Oncogene Proteins c-myc
  • Tumor Suppressor Protein p53
  • Tumor Suppressor Proteins