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miR-155 in acute myeloid leukemia: not merely a prognostic marker?

MicroRNAs (miRNAs) are critical regulators of cellular processes such as differentiation and development, proliferation, and apoptosis. Misregulation of miRNAs can cause cancer, and miRNA expression signatures have been used to classify cancers. miR-155 is one of the most frequently upregulated miRNAs in cancers; it has been linked to a variety of human lymphomas and leukemias as well as to solid tumors of the breast, colon, and lungs. In the report accompanying this article in Journal of Clinical Oncology, Marcucci et al demonstrate that miR-155 expression is an independent prognostic marker for patients with cytogenetically normal acute myeloid leukemia (AML). Patients with higher miR-155 expression experience significantly lower rates of complete remission and shorter disease-free and overall survival. Moreover, the authors describe a miR-155–associated gene expression signature that is enriched for genes involved in survival, proliferation, and inflammation. These findings highlight the potential of miR-155 as a prognostic marker and suggest it may also be a therapeutic target (ie, theranostic molecule) in AML. miR-155 has established roles in maintaining homeostatic regulatory loops in the immune system, and its increased expression may promote leukemogenesis. One critical function of miR-155 is to promote myeloid lineage commitment in hematopoietic stem cells and myeloid progenitors (Fig 1A). In these cells, inflammatory stimuli such as Toll-like receptor ligands lead to transcriptional activation of miR-155, most likely through the AP-1 and nuclear factor B transcription factors, which have been shown to regulate miR-155 expression after lipopolysaccharide stimulation in macrophages. Thus,