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Review
. 2023 Dec 30;13(1):84.
doi: 10.3390/cells13010084.

miR-142: A Master Regulator in Hematological Malignancies and Therapeutic Opportunities

Wilson Huang  1 , Doru Paul  2 , George A Calin  1   3   4 , Recep Bayraktar  3
Affiliations
Review

miR-142: A Master Regulator in Hematological Malignancies and Therapeutic Opportunities

Wilson Huang et al. Cells. .

Abstract

MicroRNAs (miRNAs) are a type of non-coding RNA whose dysregulation is frequently associated with the onset and progression of human cancers. miR-142, an ultra-conserved miRNA with both active -3p and -5p mature strands and wide-ranging physiological targets, has been the subject of countless studies over the years. Due to its preferential expression in hematopoietic cells, miR-142 has been found to be associated with numerous types of lymphomas and leukemias. This review elucidates the multifaceted role of miR-142 in human physiology, its influence on hematopoiesis and hematopoietic cells, and its intriguing involvement in exosome-mediated miR-142 transport. Moreover, we offer a comprehensive exploration of the genetic and molecular landscape of the miR-142 genomic locus, highlighting its mutations and dysregulation within hematological malignancies. Finally, we discuss potential avenues for harnessing the therapeutic potential of miR-142 in the context of hematological malignancies.

Keywords: cancer; exosome; hematopoiesis; leukemia; lymphoma; miR-142; microRNA; mutation; non-coding RNA; physiology.

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Conflict of interest statement

G.A.C. is the scientific founder of Ithax Pharmaceuticals, Inc. The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Components and relative positions of the secondary stem-loop structure of the pre-miR-142 sequence. The circles represent nucleotides; the circles’ colors correspond to the component of pre-miR-142. Each colored number corresponds to the nucleotide position relative to the specific component of pre-miR-142.
Figure 2
Figure 2
Biogenesis and regulation of miR-142. The transcription of the MIR142HG gene via RNA polymerase II/III is regulated by proteins, including CLOCK/BMAL1, PU.1, Runx1, and C/EBP transcriptional promotion and p300 and MAPK transcriptional repression, dependent on the cell type or larger function of the organ system. The transcript forms the pri-miR-142 structure, which is subsequently cleaved by DGCR8 and Drosha to form pre-miR-142. This is released into the cytoplasm through the facilitation of exportin-5/Ran-GTP and processed via TRBP and Dicer to generate the mature miR-142 duplex. Either one or both mature miR-142-3p and -5p strands can be incorporated into the RNA-induced silencing complex (RISC) to enact post-transcriptional regulation by targeting mRNAs. The binding of the miRNA RISC complex leads to either mRNA degradation or translational inhibition.
Figure 3
Figure 3
The effects of miR-142 deficiency on hematopoiesis and hematopoietic cells, including B cells, T cells, natural killer (NK) cells, and myeloid cells. Affected targets and downregulated or upregulated signaling pathways are shown.
Figure 4
Figure 4
Mutations identified within the secondary stem-loop structure of the pre-miR-142 sequence. The circles represent nucleotides. Point mutations found in hematological malignancies described in this article are indicated by arrows with nucleotides encased in squares; the squares’ colors correspond to the cancer type. The components of pre-miR-142, which include the mature 3p strand, 5p strand, and seed sequence, are as depicted in Figure 1 (the miR-142-5p sequence is represented by nucleotides encased in blue circles, the miR-142-3p sequence is represented by nucleotides encased in green circles, and the seed sequences in each mature sequence are represented by nucleotides in red circles).
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