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
Published online Jun 24, 2020. doi: 10.5306/wjco.v11.i6.348
miRNA name | Description | Ref. |
hsa-let-7b | In 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-17 | Differential 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-100 | miR-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-101 | Hsp90 co-chaperone – p23, is regulated by hsa-miR-101, which is downregulated in childhood ALL cases | [156] |
hsa-mir-124 | miR-124 contributes to glucocorticoid resistance in acute lymphoblastic leukemia by promoting proliferation, inhibiting apoptosis, and targeting the glucocorticoid receptor | [157] |
hsa-mir-126 | miR-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-142 | Upregulation 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-181a | Ectopic 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-181a | miR-181a play role as negative regulator for the TGF-β1 signaling pathway | [47] |
hsa-mir-196b | miR-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-1290 | miR196b 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-222 | Overexpression 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 h | POLD1 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-595 | miR-595 suppresses the cellular uptake and cytotoxic effects of methotrexate by targeting SLC19A1 in CEM/C1 cells | [164] |
hsa-mir-664 | miR-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-708 | The 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-2909 | The 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] |
- Citation: Szczepanek J. Role of microRNA dysregulation in childhood acute leukemias: Diagnostics, monitoring and therapeutics: A comprehensive review. World J Clin Oncol 2020; 11(6): 348-369
- URL: https://www.wjgnet.com/2218-4333/full/v11/i6/348.htm
- DOI: https://dx.doi.org/10.5306/wjco.v11.i6.348