MiR-92a inhibits fibroblast-like synoviocyte proliferation and migration in rheumatoid arthritis by targeting AKT2

Yu, Fangyuan; Xie, Congqin; Jiang, Changliang; Sun, Jitong; Feng, Hui-cheng; Li, Chao; Huang, Xunwu

doi:10.1007/s12038-018-9803-0

Cited by 11 publications

(7 citation statements)

References 35 publications

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“…miRNA has attracted widespread attention over the past decade (11), due to reports of a large quantity of aberrantly expressed miRNAs associated with the pathogenesis of RA (29–32). Studying the abnormal expression of these miRNAs in RA can potentially facilitate the understanding of RA pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

Role and mechanism of miR‑144‑5p in LPS‑induced macrophages

Zhou

et al. 2019

Exp Ther Med

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The aim of the present study was to explore the possible role of microRNA-144-5p (miR-144-5p) in rheumatoid arthritis (RA) and the associated mechanism. Following the induction of THP-1 cell differentiation into macrophages by phorbol ester (100 ng/ml) treatment, an in vitro inflammatory model of RA was established by treating the THP-1 macrophages with 1 µg/ml lipopolysaccharide (LPS). The level of miR-144-5p was subsequently measured using reverse transcription-quantitative PCR, which found that the expression of miR-144-5p was significantly reduced in LPS-treated THP-1 macrophages. Bioinformatics analysis and a dual-luciferase reporter assay were used to predict and confirm TLR2 as a direct target of miR-144-5p, respectively. Toll-like receptor 2 (TLR2) was then validated as a target gene of miR-144-5p. The effects of miR-144-5p upregulation and TLR2 silencing on LPS-treated THP-1 macrophages were then determined by transfection with miR-144-5p mimic and TLR2-siRNA, respectively. Cell viability was subsequently measured using a Cell Counting Kit-8 assay, whilst the expression of tumor necrosis factor-α (TNF-α), interleukin (IL)-6 and IL-8 secreted by THP-1 macrophages was measured using ELISA. Western blotting was performed to measure p65 phosphorylation (p-p65) in the NK-κB signaling pathway. It was found that miR-144-5p overexpression reduced macrophage cell viability, reduced the expression of TNF-α, IL-6 and IL-8, and reduced the expression of TLR2 and p-p65 compared with the control group. Likewise, TLR2 silencing also reduced macrophage cell viability and reduced the expression of TNF-α, IL-6 and IL-8 in THP-1 macrophages. In conclusion, the data from the present study suggested that miR-144-5p overexpression reduced THP-1 macrophage cell viability and inhibited the expression of TNF-α, IL-6 and IL-8 in cells, possibly by inhibiting the expression of TLR2 and suppressing the activation of NK-κB signaling. Therefore, miR-144-5p may serve as a novel therapeutic target for the treatment of RA.

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Section: Discussionmentioning

confidence: 99%

Role and mechanism of miR‑144‑5p in LPS‑induced macrophages

Zhou

et al. 2019

Exp Ther Med

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“…Moreover, the CXCL9/CXCR3 axis promoted invasion and metastasis through AKT2-mediated epithelial-mesenchymal transition in tongue squamous cell carcinoma (35). Since AKT2 mRNA has been demonstrated to be regulated by diverse miRNAs, such as miR-194 (36), miR-625-5p (37) and miR-92a (38), the crosstalk of these miRNAs that controls the translational repression of AKT2 requires further exploration.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑149‑3p inhibits cell proliferation by targeting AKT2 in oral squamous cell carcinoma

et al. 2020

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“…Aberrant expression of miRNAs has been detected in RAassociated in ammatory innate immune responses, and they are increasingly being considered as prognostic biomarkers as well as therapeutic targets [12,13]. For example, Yu et al showed that miR-92a could target AKT2 to inhibit broblast-like synoviocyte proliferation and migration in RA [14]. Liu et al found a decreased miR-125 level in synovial tissues, and miR-125 may regulate PI3K/Akt/mTOR pathway by directly inhibiting PARP2 expression, thereby weakening the development of RA [15].…”

Section: Discussionmentioning

confidence: 99%

MiRNA-6089 inhibits rheumatoid arthritis fibroblast-like synoviocytes proliferation and induces apoptosis by targeting CCR4

Lin

Wang

Zhang

et al. 2020

Archives of Physiology and Biochemistry

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Background: Growing data have indicated that broblast-like synoviocytes (FLS) and miRNAs are implicated in the pathogenesis of rheumatoid arthritis (RA). This study was aimed to evaluate the function of miR-6089 in the regulation of RA-FLSs. Methods: The expression of miR-6089 was measured by quantitative real time PCR (qRT-PCR). The RA-FLSs were transfected with si-CCR4 plasmids or miR-6089 mimic, and subjected to CCK-8 and ow cytometry to analyze proliferation and apoptosis. The concentrations of MMP-1, TNF-α and IL-6 in RA-FLSs supernatant were detected using ELISA. The protein expression of caspase-3,-8 and-9 was detected using western blot. Results: The levels of miR-6089 were detected to be signi cantly lower in the synovial tissues and FLSs of RA than in the synovial tissues and FLSs of healthy controls. The miR-6089 up-regulation in RA-FLSs signi cantly inhibited the proliferation and promoted cell apoptosis accompany with an increase protein expression of caspase-3,-8 and-9. Furthermore, CCR4 was determined to directly target miR-6089, and its expression was signi cantly increased in the synovial tissues of RA than in the synovial tissues of healthy controls. Moreover, CCR4 overexpression effectively reversed the effect on proliferation and apoptosis induced by miR-6089 in RA-FLSs. Conclusion: Our results revealed that miR-6089 may be a potential target for RA prevention and therapy of RA.

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MiR-92a inhibits fibroblast-like synoviocyte proliferation and migration in rheumatoid arthritis by targeting AKT2

Cited by 11 publications

References 35 publications

Role and mechanism of miR‑144‑5p in LPS‑induced macrophages

Role and mechanism of miR‑144‑5p in LPS‑induced macrophages

MicroRNA‑149‑3p inhibits cell proliferation by targeting AKT2 in oral squamous cell carcinoma

MiRNA-6089 inhibits rheumatoid arthritis fibroblast-like synoviocytes proliferation and induces apoptosis by targeting CCR4

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