The MicroRNA Family Both in Normal Development and in Different Diseases: The miR-17-92 Cluster

Abstract

An increasing number of research studies over recent years have focused on the function of microRNA (miRNA) molecules which have unique characteristics in terms of structure and function. They represent a class of endogenous noncoding single-strand small molecules. An abundance of miRNA clusters has been found in the genomes of various organisms often located in a polycistron. The miR-17-92 family is among the most famous miRNAs and has been identified as an oncogene. The functions of this cluster, together with the seven individual molecules that it comprises, are most related to cancers, so it would not be surprising that they are considered to have involvement in the development of tumors. The miR-17-92 cluster is therefore expected not only to be a tumor marker, but also to perform an important role in the early diagnosis of those diseases and possibly also be a target for tumor biotherapy. The miR-17-92 cluster affects the development of disease by regulating many related cellular processes and multiple target genes. Interestingly, it also has important roles that cannot be ignored in disease of the nervous system and circulation and modulates the growth and development of bone. Therefore, it provides new opportunities for disease prevention, clinical diagnosis, prognosis, and targeted therapy. Here we review the role of the miR-17-92 cluster that has received little attention in relation to neurological diseases, cardiac diseases, and the development of bone and tumors.

MiR‐17‐3p inhibits osteoblast differentiation by downregulating Sox6 expression

“…We used these cells in the present study to investigate the mechanism by which miR-17-3p regulates osteoblast differentiation. Interestingly, the miR-17-92 cluster has been shown to regulate bone growth and development; as a mature miRNA within this cluster, miR-17-3p has been suggested to play an essential role in bone formation [25], which is supported by the current findings.…”

Cell-to-Cell Communication in Learning and Memory: From Neuro- and Glio-Transmission to Information Exchange Mediated by Extracellular Vesicles

“…Much evidence suggests that these cell-to-cell communications rely, at least in part, on different classes of EVs. miR-9-derived miR-9-3p [226] Dystrophin [226]; Voltage-dependent Calcium channel, g subunit [226,227]; Leucine rich repeat transmembrane neuronal 1 [226,228]; Cadherin 2 [226,229]; Fibronectin [230]; Calcineurin B, type I [226,231] Regulates synaptic plasticity and memory [226] Found in serum exosomes of acute ischemic stroke patients [217] miR-17-92 cluster: miR-17, miR-18a, miR-19a, miR-19b, miR-20a, and miR-92a [213,[232][233][234] Phosphatase and Tensin Homolog (PTEN) [211,234] -Regulate axonal outgrowth in development [211]; -Regulate adult hippocampal neurogenesis, anxiety, and depression [232]; -Enhance neuroplasticity and functional recovery after stroke [233,234]; -Enhance neurite remodeling, neurogenesis and angiogenesis in post-stroke rats [233]; -Ablation in mouse impairs hippocampal-dependent learning and memory [212] miR-19a found in exosomes [213,233] miR-26a [209] PTEN, GSK-3, BDNF [209] Stimulates neurite/axonal elongation [209] Found in astrocytic exosomes [209] miR-29c [235] Beta secretase 1 (BACE1) [236] This microRNA can be an endogenous regulator of the BACE 1 enzyme, and thus of beta amyloid precursor protein (APP) metabolism. [236] Found in exosomes contained in frozen post-mortem prefrontal cortex from bipolar individuals [235] miR-34a [237]<...>…”

Hsa-mir-210 as a novel signature predicts survival in lung squamous cell carcinoma using bioinformatics analysis

“…For example, the down-regulated expression of hsa-mir-199 in lung cancer is closely related to staging, distant metastasis and poor prognosis, and may inhibit the malignant progression of lung cancer by interacting with RGS 17 [17]; hsa-mir-30e plays an inhibitory role in NSCLC, and may inhibit cell proliferation and invasion by directly targeting SOX 9 [18]; The hsa-mir-451 regulates survival of NSCLC cells partially through the downregulation of RAB14 and targeting with the hsa-mir--451/RAB14 interaction might serve as a novel therapeutic application to treat NSCLC patients [19]. In addition, hsa-mir-373 [20], hsa-mir-17-92 cluster [21,22], hsa-mir-21 [23], hsa-mir-126 [24], hsa-mir-145 [25], and hsa-mir-340 [26] were also found to be closely related to the occurrence, progression and survival of lung cancer.…”