A Potential Link between hnRNP K and Cebpα: Implications for Ribosomal Dysfunction in Acute Myeloid Leukemia (AML)

Deletion of the long arm of chromosome 9, del(9q), is a recurrent genetic abnormality involving the haploinsufficient loss of the RNA binding protein hnRNPK and is often associated with poor treatment responses in AML. In addition to reduced hnRNP K expression, other critical proteins, not localized to this locus, are also aberrantly expressed in del9q AML. One protein of critical interest is CEBPα, a well-established myeloid differentiation transcription factor. Recently, CEBPα was discovered to have a novel role in ribosomal RNA (rRNA) synthesis. However, as opposed to CEBPα, hnRNP K's role in RNA stability, rRNA processing, and ribosomal functions is already firmly rooted. Collectively, these results suggest that del(9q) AML dysregulations in hnRNP K and CEBPα expression may have a multi-faceted influence on ribosomal biogenesis and protein translation.