Table 2.
HSCs aging-related miRNAs and their miRNA target(s)
| MicroRNA | mRNA Targets | Description | References |
|---|---|---|---|
| miR-212/132 cluster | FOXO3 | miR-132 utilized its efficacy on senescence HSCs by targeting the transcription agent FOXO3, a recognized aging-related gene. In addition, these miRNAs have a function in preserving balanced HSCs output | [126] |
| miR-125b | HOXA1 | Overexpression of miR-125b alters the HSC compartment composition by providing HSCs with a more stress-resistant and anti-apoptotic environment, resulting in an increase frequency of the CD150low "lineage balanced" and CD150neg lymphoid-biased HSC subsets | [127–129] |
| miR-33 | p53 | Defining the function of miR-33 in regulating the HSC self-renewal via p53 may result in the inhibition and therapy of hematopoietic disorders | [130] |
| miR-146a | TRAF6 | Therefore, loss of miR-146a controls cell-extrinsic and -intrinsic pathways associating HSC inflammation to the development of AML | [133] |
| miR-139 − 5p | BRG1 | miR-139-5p is a crucial modulator of cellular proliferation in primary hematopoiesis and is a strong antileukemic molecule | [138] |
| miR-126 | CDK3 | miR-126 targets the PI3K/AKT/mTOR signaling pathway, protecting AML stem cell quiescence and promoting antineoplastic resistance | [128, 136] |
| miR-193b | c-KIT | Ectopic miR-193b expression limits long-time repopulating HSC development and blood regeneration. miR-193b-defective HSCs and pHSCs show enhanced basic and cytokine-stimulated STAT5 and AKT signaling. This STAT5-stimulated miRNA provides negative feedback for extreme signaling to limit unregulated HSC increase | [139] |
| miR-382 − 5p | MXD1 | miR-382-5p overexpression in CD34 + HSCs/pHSCs results in a remarkable reduction of megakaryocyte precursors coupled to augment granulocyte ones | [140] |
| miR-155 | CXCL12 | miR-155 enhances G-CSF-stimulated mobilization of murine HSCs and pHSCs through the propagation of CXCL12 signaling | [141] |
| miR-143/145 | TGFβ | miR-143/145 plays a cell context-related function in HSPC action via control of TGFβ/DAB2 triggering, and lack of these miRNAs generates a preleukemic condition | [142] |