The Glucose-Regulated MiR-483-3p Influences Key Signaling Pathways in Cancer

Pepe, Felice; Visone, Rosa; Veronese, Angelo

doi:10.3390/cancers10060181

Cited by 42 publications

(32 citation statements)

References 134 publications

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“…In cancer studies, miR-483-3p was also found to affect the Wnt/β-catenin and TGF-β signaling pathways via modulating several genes Pepe, Visone, & Veronese, 2018). The aforementioned studies show that the regulation of miR-483 is diverse and the context extensive.…”

Section: Discussionmentioning

confidence: 99%

miR‐483 inhibits bovine myoblast cell proliferation and differentiation via IGF1/PI3K/AKT signal pathway

Song

Dong

et al. 2018

Journal Cellular Physiology

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MicroRNAs (miRNAs) have been established to regulate skeletal muscle development in mammals. However, few studies have been conducted on the regulation of proliferation and differentiation of bovine myoblast cells by miRNAs. The aim of our study was to explore the function of miR‐483 in cell proliferation and differentiation of bovine myoblast. Here, we found that miR‐483 declined in both proliferation and differentiation stages of bovine myoblast cells. During the proliferation phase, the overexpression of miR‐483 downregulated the cell cycle–associated genes cyclin‐dependent kinase 2 (CDK2), proliferating cell nuclear antigen (PCNA) messenger RNA (mRNA), and the protein levels. At the cellular level, cell cycle, cell counting kit‐8, and 5‐ethynyl‐2´‐deoxyuridine results indicated that the overexpression of miR‐483 block cell proliferation. During differentiation, the overexpression of miR‐483 led to a decrease in the levels of the myogenic marker genes MyoD1 and MyoG mRNA and protein. Furthermore, the immunofluorescence analysis results showed that the number of MyHC‐positive myotubes was reduced. In contrast, the opposite experimental results were obtained concerning both proliferation and differentiation after the inhibition of miR‐483. Mechanistically, we demonstrated that miR‐483 target insulin‐like growth factor 1 (IGF1) and downregulated the expression of key proteins in the PI3K/AKT signaling pathway. Altogether, our findings indicate that miR‐483 acts as a negative regulator of bovine myoblast cell proliferation and differentiation.

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Section: Discussionmentioning

confidence: 99%

miR‐483 inhibits bovine myoblast cell proliferation and differentiation via IGF1/PI3K/AKT signal pathway

Song

Dong

et al. 2018

Journal Cellular Physiology

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“…Bioinformatic analysis and luciferase reporter assay discovered that hsa_circ_0123190 directly bind to hsa-miR-483-3p, which serves as a miRNA sponge. There have been several reports that increased hsa-miR-483-3p impair endothelial cell survival to limit vascular repair capacity upon injury in cancer and metabolic diseases [24][25][26]. However, the role of hsa-miR-483-3p has been unreported in LN, which also has vascular lesion.…”

Section: Discussionmentioning

confidence: 99%

Hsa_circ_0123190 acts as a competitive endogenous RNA to regulate APLNR expression by sponging hsa-miR-483-3p in lupus nephritis

Zhang

Gao

et al. 2020

Preprint

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Background Lupus nephritis (LN) is one of the most severe complications of systemic lupus erythematosus (SLE). Circular RNAs(circRNAs) can act as competitive endogenous RNAs (ceRNAs) to regulate gene transcription, which is involved in mechanism of many diseases. However, the role of circRNA in lupus nephritis has been rarely reported. In this study, we aim to investigate the clinical value of circRNAs and explore the mechanism of circRNA involvement in the pathogenesis of LN. Methods Renal tissues from three untreated LN patients and three normal controls (NCs) were used to identify differently expressed circRNAs by next-generation sequencing (NGS). Validated assays were used by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The interactions between circRNA and miRNA, or miRNA and mRNA were further determined by luciferase reporter assay. The extent of renal fibrosis between the two groups was assessed by Masson-trichome staining and immunohistochemistry (IHC) staining. Results 159 circRNAs were significantly dysregulated in LN patients compared with NCs. The expression of hsa_circ_0123190 was significantly decreased in renal tissues of patients with LN (P = 0.014). Bio-informatic analysis and luciferase reporter assay illustrated that hsa_circ_0123190 can act as a sponge for hsa-miR-483-3p, which was also validated to interact with APLNR. APLNR mRNA expression was related with chronicity index (CI) of LN (P = 0.033, R2 = 0.452). Moreover, the fibrotic-related protein, transforming growth factor-β1 (TGF-β1), which was regulated by APLNR, was more pronounced in the LN group (P = 0.018). Conclusion Hsa_circ_0123190 may function as a ceRNA to regulate APLNR expression by sponging hsa-miR-483-3p in LN.

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“…However, the function of micro-483-5p (miR-483-5p) in ovarian was little known. Moreover, several studies have shown that miR-483-5p is associated with the progression of various cancers [25]. For example, the modulation of miR-483-5p levels may increase CDDP sensitivity in tongue squamous cell carcinoma (TSCC) cells through a novel mitochondrial ssion pathway [26].…”

Section: Introductionmentioning

confidence: 99%

Elevated levels of miR-483-5p in oocytes aggravates premature ovarian insufficiency induced by CDDP by targeting the FKBP4

Zhao

Ouyang³

et al. 2020

Preprint

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Background: Premature ovarian insufficiency (POI) is characterized by a loss of ovarian function before 40 years-of-age and represents an existing challenge cause of female infertility. POI is one of the dominant causes of cis-diaminedichloroplatinum (cisplatin, CDDP)-induced reproductive impairment. However, the detailed mechanisms underlying POI induced by CDDP remain unclear.Methods: The POI C57B6/J mouse model was created by administering CDDP. The effects of FKBP4 were investigated using isobaric tags for relative and absolute quantification analysis (iTRAQ), real-time quantitative PCR (qRT-PCR) and western blotting. Target prediction was predicted using TargetScan software. Levels of sex hormones were tested using Enzyme-linked immunosorbent assays (ELISA).Results: We found that the FKBP4 protein was down-regulated in the ovaries of CDDP model. Target prediction identified FKBP4 as a potential target for miR-483-5p, which was expressed at high levels in both the ovaries and serum of CDDP-POI mice, and in the serum from POI patients. In vitro experiments further confirmed that FKBP4 was the target for miR-483-5p in human cervical cancer cells (HeLa). The overexpression of FKBP4 in human granulosa cells (KGN) alleviated the apoptosis caused by CDDP and the overexpression of miR-483-5p. Furthermore, the overexpression of miR-483-5p in oocytes caused injury to the ovaries, and disrupted the levels of sex hormones in CDDP-POI mice (AMH: P < 0.01; E2: P < 0.01; FSH: P < 0.01).Conclusions: Analyses showed that miR-483-5p targets the FKBP4 protein in a mouse model of POI induced by CDDP. Elevated levels of miR-483-5p in oocytes could aggravate POI induced by CDDP by targeting FKBP4. Overall, our data demonstrate that miR-483-5p was responsible for the underlying pathophysiology of POI induced by chemotherapeutic treatments, such as CDDP.

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The Glucose-Regulated MiR-483-3p Influences Key Signaling Pathways in Cancer

Cited by 42 publications

References 134 publications

miR‐483 inhibits bovine myoblast cell proliferation and differentiation via IGF1/PI3K/AKT signal pathway

miR‐483 inhibits bovine myoblast cell proliferation and differentiation via IGF1/PI3K/AKT signal pathway

Hsa_circ_0123190 acts as a competitive endogenous RNA to regulate APLNR expression by sponging hsa-miR-483-3p in lupus nephritis

Elevated levels of miR-483-5p in oocytes aggravates premature ovarian insufficiency induced by CDDP by targeting the FKBP4

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