Review
Copyright ©The Author(s) 2020.
World J Clin Oncol. Jun 24, 2020; 11(6): 348-369
Published online Jun 24, 2020. doi: 10.5306/wjco.v11.i6.348
Table 1 Targets of microRNA associated with acute leukemia (based on data in Human microRNA Disease Database http://www.cuilab.cn/hmdd)
miRNA nameDescriptionRef.
hsa-let-7bIn patients with ALL, the expression of microRNA let-7b is regulated by methylation of CpG islands in the region of the genomic promoter. The microRNA let-7b may act as a tumor suppressor, whose low expression is involved in ALL development, indicating the microRNA let-7b may become a new therapeutic target for ALL[154]
hsa-mir-17Differential expression of miR-17~92 identifies BCL2 as a therapeutic target in BCR-ABL-positive B-lineage acute lymphoblastic leukemia[155]
hsa-mir-99a, hsa-mir-100miR-100 and miR-99a have critical roles in altering cellular processes by targeting both the FKBP51 and IGF1R/mTOR signaling pathways in vitro and might represent a potential novel strategy for ALL treatment[43]
hsa-mir-101Hsp90 co-chaperone – p23, is regulated by hsa-miR-101, which is downregulated in childhood ALL cases[156]
hsa-mir-124miR-124 contributes to glucocorticoid resistance in acute lymphoblastic leukemia by promoting proliferation, inhibiting apoptosis, and targeting the glucocorticoid receptor[157]
hsa-mir-126miR-126 plays a critical but 2-faceted role in leukemia and thereby uncovers a new layer of miRNA regulation in cancer. miR-126 depletion can sensitize AML cells to standard chemotherapy, which suggests that miR-126 represents a promising therapeutic target[158]
hsa-mir-142Upregulation of miR-142-3p decreased MLL-AF4 expression in the RS4;11 leukemic cell line. Ectopic expression of miR-142-3p remarkably suppressed cell proliferation and induced apoptosis, and exogenous expression of miR-142-3p strongly reduced the expression of MLL-AF4 target genes such as homeobox A HOXA9, HOXA7, and HOXA10[159]
hsa-mir-181aEctopic expression of miR-181a resulted in decreased CD10 hyperexpression in ETV6/RUNX1+ primary patient samples. miR-181a could target ETV6/RUNX1 and cause a reduction in the level of that oncoprotein, cell growth arrest, an increase in apoptosis, and induction of cell differentiation in ETV6/RUNX1+ cell line[48]
hsa-mir-181amiR-181a play role as negative regulator for the TGF-β1 signaling pathway[47]
hsa-mir-196bmiR-196b becomes nonfunctional in T-cell ALL as a consequence of mutations in 3'-UTR of the c-myc gene in T-cell ALL cellular models[160]
hsa-mir-196b, hsa-mir-1290miR196b and miR-1290 target the IGFBP3 3'-UTR and participate in the antitumor effect of resveratrol via regulation of IGFBP3 expression in acute lymphoblastic leukemia. miR-196b/miR-1290 are potential therapeutic targets for ALL[161]
hsa-mir-221 hsa-mir-222Overexpression of miR-221 in ALL cells prompted cell-cycle progression and sensitization of ALL cells to cytotoxic agents. Niche-influenced miR-221/222 may define a novel therapeutic target in ALL[162]
hsa-mir-520 hPOLD1 and MCM2 were found to be regulated by miR-520H via E2F1. High expression of POLD1, MCM2, and PLK4 might play positive roles in the recurrence of ALL[163]
hsa-mir-595miR-595 suppresses the cellular uptake and cytotoxic effects of methotrexate by targeting SLC19A1 in CEM/C1 cells[164]
hsa-mir-664miR-664 negatively regulates PLP2 and promotes cell proliferation and invasion in T-cell acute lymphoblastic leukemia. miR-664 may represent a potential therapeutic target for T-ALL intervention[115]
hsa-mir-708The expression level of miR-708 reflects differences among the clinical types of common-ALL, and CNTFR, NNAT, and GNG12 were identified as targets of miR-708[165]
hsa-mir-2909The miR-2909-KLF4 molecular axis is able to differentiate between the pathogeneses of pediatric B- and T-cell ALLs, which may represent a new diagnostic/prognostic marker[166]