miR-192 Directly Binds and Regulates Dicer1 Expression in Neuroblastoma

Feinberg-Gorenshtein, Galina; Guedj, Avital; Shichrur, Keren; Jeison, Marta; Luria, Drorit; Kodman, Yona; Ash, Susan; Feinmesser, Meora; Edry, Liat; Shomron, Noam; Weizman, Abraham; Yaniv, Isaac; Avigad, Smadar

doi:10.1371/journal.pone.0078713

Cited by 39 publications

(26 citation statements)

References 25 publications

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“…It has been reported that miR-192 was downregulated in colon cancer, osteosarcoma, and bladder cancer [9][10][11]. However, upregulation of miR-192 was found in pancreatic ductal adenocarcinoma, neuroblastoma, and gastric cancer [12][13][14]. It indicted that the abnormal expression of miR-192 has tissue specificity in human cancers.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-192 promotes the development of nasopharyngeal carcinoma through targeting RB1 and activating PI3K/AKT pathway

Huang

Hou²,

Zhu

et al. 2020

World J Surg Onc

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Background: The dysregulation of microRNAs (miRNAs) has been found in diseases and cancers, including microRNA-192 (miR-192). This study was designed to investigate the role of miR-192 in nasopharyngeal carcinoma (NPC) progression. Methods: The expression levels of miR-192 and some genes were assessed by qRT-PCR and Western blot. The function of miR-192 was investigated through MTT, Transwell, and dual-luciferase reporter assays. Results: The expression of miR-192 was increased in NPC tissues, and high miR-192 expression predicted poor prognosis in NPC patients. Functionally, upregulation of miR-192 promoted NPC cell migration, invasion, and growth. Furthermore, miR-192 activated EMT and PI3K/AKT pathway to regulate NPC progression. In addition, miR-192 directly targeted RB1 and suppressed its expression in NPC. Moreover, overexpression of RB1 weakened the promoted effect of miR-192 in NPC. Conclusion: miR-192 promoted cell viability and metastasis in NPC through suppressing RB1 expression and activating PI3K/AKT pathway.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-192 promotes the development of nasopharyngeal carcinoma through targeting RB1 and activating PI3K/AKT pathway

Huang

Hou²,

Zhu

et al. 2020

World J Surg Onc

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“…More, recently, miRs have been reported to affect the development of depression and have been used as an antidepressant treatment approach (13,14), in connection with their regulation of the development and function of the nervous system (15,16). Notably, miR-192 has been shown to play an important role in neuroblastoma, a malignancy that shares a close correlation with depression (17,18). miR-192, -197, and -346 have been found to be highly expressed in follicular thyroid carcinoma, and EGF containing Fibulin (Fbln) extracellular matrix protein-2 (Fbln-4) is suppressed by overexpressed miR-346, indicating that miR-192 may be associated with Fbln-4 (19).…”

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confidence: 99%

Up‐regulated miR‐192‐5p expression rescues cognitive impairment and restores neural function in mice with depression via the Fbln2‐mediated TGF‐β1 signaling pathway

et al. 2018

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Depression represents a condition characterized by cognitive deficits and neural dysfunction and has recently been correlated with microRNAs (miRs) and their respective target genes. The present study was conducted with the goal of investigating the expression of miR-192-5p and its target gene fibulin (Fbln)-2 in an attempt to evaluate their roles in the occurrence and progression of cognitive impairment and neural function in mice with chronic unpredictable mild stress (CUMS)-induced depression through regulation of the TGF-β1 signal transduction pathway. Verification of the targeting relationship between miR-192-5p and Fbln2 was provided in the form of initial bioinformatics prediction, followed by a further verification in the form of a dual-luciferase reporter gene assay. Normal mice and models induced by CUMS were assigned into various groups, whereas mimics, inhibitors, and small interfering RNA were introduced to validate the regulatory mechanism by which miR-192-5p regulates Fbln2 depression. Novel object recognition, tail suspension testing, and Morris water maze were all employed 28 d after transfection. Hippocampal electrophysiological recordings, Golgi staining, HPLC mass spectrometry, and fluorescence immunohistochemistry were performed to further evaluate cognitive function and neuron regeneration. CUMS-induced depression was determined to represent a predisposing factor for cognitive impairment and damage to neural function in mice, highlighted by novel object recognition, learning and memory abilities, population spike amplitude, synaptic transmission, cAMP levels, neuronal regeneration, and increased behavioral changes that resemble depression. Furthermore, increased Fbln2 expression, an activated TGF-β1 signaling pathway, and decreased expression of miR-192-5p, synaptophysin, brain-derived neurotrophic factor, N-methyl-d-aspartate receptor subunit 2B, and calmodulin-dependent protein kinase II were noted. Up-regulated miR-192-5p targeting Fbln2 acts to alleviate CUMS-induced depression by inhibiting the TGF-β1 signaling pathway, resulting in the enhanced cognitive function in novel object recognition, learning and memory ability, population spike amplitude, synaptic transmission, neuron regeneration, and alleviation of behavioral symptoms. The central findings of the present study indicate that up-regulated levels of miR-192-5p expression act to suppress activation of the TGF-β1 signaling pathway by means of binding to Fbln2, thereby ameliorating cognitive impairment and strengthening neural function in a mouse model of depression.-Tang, C.-Z., Yang, J.-T., Liu, Q.-H., Wang, Y.-R., Wang, W.-S. Up-regulated miR-192-5p expression rescues cognitive impairment and restores neural function in mice with depression via the Fbln2-mediated TGF-β1 signaling pathway.

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“…The MIR192 gene is transcribed together with miR-194 [7]. Several studies reported the upregulation of miR-192 in different cancer types, including gastric cancer, hepatocellular carcinoma, and neuroblastoma [8][9][10]. Conversely, miR-192 was downregulated in colorectal cancer and hematological disorders, as well as in lymphoblastic leukemia (ALL) where it was associated with poor prognosis (Supplemental Table 1) [11,12].…”

Section: Introductionmentioning

confidence: 99%

Tumor suppressive function of microRNA-192 in acute lymphoblastic leukemia

Sayadi

Ajdary

Nadali

et al. 2017

Bosn J of Basic Med Sci

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Non-coding RNAs play a critical role in gene regulation in cancer cells. Reduced expression of microRNA-192 (miR-192) has been detected in many cancers. In this study, we investigated the role of miR-192 in cell proliferation and cell cycle control in NALM-6 cell line, a model of acute lymphoblastic leukemia (ALL). Cell cycle analysis by DNA content using propidium iodide staining and cell apoptosis analysis using Annexin V assay were carried out. Cell proliferation changes were monitored using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. In addition, the relative changes in P53, BAX, CASP3, and BCL-2 gene expression were determined by quantitative reverse transcription PCR. Overexpression of miR-192 resulted in cell proliferation arrest in ALL cells. After 72 and 96 hours of transduction, apoptosis was significantly increased in the cells transduced with miR-192-overexpressing virus compared with control cells. The expression of P53, BAX, and CASP3 increased after 48 hours of transduction in miR-192-overexpressing cells, but no change was observed in BCL-2 expression. The G0/S and G1/S ratio changed to 7.5 and 4.5, respectively, in the cells overexpressing miR-192 compared with controls. The results of our study suggest, for the first time, tumor suppressive effects of miR-192 in ALL cells.

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miR-192 Directly Binds and Regulates Dicer1 Expression in Neuroblastoma

Cited by 39 publications

References 25 publications

MicroRNA-192 promotes the development of nasopharyngeal carcinoma through targeting RB1 and activating PI3K/AKT pathway

MicroRNA-192 promotes the development of nasopharyngeal carcinoma through targeting RB1 and activating PI3K/AKT pathway

Up‐regulated miR‐192‐5p expression rescues cognitive impairment and restores neural function in mice with depression via the Fbln2‐mediated TGF‐β1 signaling pathway

Tumor suppressive function of microRNA-192 in acute lymphoblastic leukemia

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