The present study aimed to explore the expression and effects of microRNA (miR)-155 in synovial fibroblasts of patients with rheumatoid arthritis (RA). A total of 89 synovial tissues from RA patients and 49 control synovial tissues were collected, and the levels of miR-155 were measured by reverse transcription quantitative-PCR and western blotting. Fibroblast-like synoviocytes (FLS) were isolated from synovial tissues from the control group and were used to evaluate the roles of miR-155 and forkhead box protein O3a (FOXO3a). MTT assay was used to measure the proliferation of FLS. The expression of miR-155 in RA synovial tissues was significantly higher than that in the control group, but the expression of FOXO3a was significantly lower. In RA synovial tissues, miR-155 expression was negatively correlated with FOXO3a expression, but was positively correlated with the release of inflammatory cytokines interleukin (IL)-1β, IL-6 and tumor necrosis factor-α (TNF-α). A dual-luciferase reporter system showed that miR-155 inhibited the expression of FOXO3a in FLS cells. miR-155 also promoted secretion of the inflammatory cytokines IL-1β, IL-6 and TNF-α by FLS and proliferation of these cells by targeting FOXO3a.

/pdf/mir-155-promotes-fibroblast-like-synoviocyte-proliferation-1493v3xrlj.pdf

miR-155 promotes fibroblast-like synoviocyte proliferation and inflammatory cytokine secretion in rheumatoid arthritis by targeting FOXO3a

Rheumatoid arthritis (RA) is a chronic inflammatory joint disease characterized by synovial inflammation. Fibroblast‑like synoviocytes (FLS) serve a vital role in the initiation and perpetuation of the immune response in patients with RA. The present study aimed to investigate the potential role of microRNA (miR)‑34a‑3p in the pathogenesis of RA. FLS were collected from patients with RA and osteoarthritis (OA). The miR‑34a‑3p mimics and inhibitor vectors were constructed and transfected into RAFLS using Lipofectamine® 2000. Cell proliferation was determined by Cell Counting kit‑8 assay and cell cycle progression was analyzed by flow cytometry. In addition, the expression levels of cell cycle control genes, matrix metalloproteinase (MMP)‑1 and MMP‑9, and pro‑inflammatory cytokines were detected by reverse transcription‑quantitative polymerase chain reaction and western blot analysis. The potential targets of miR‑34a‑3p were predicted by TargetScan and MiRWalk; the target genes were further verified using a luciferase reporter assay. The expression levels of miR‑34a‑3p were generally lower in RAFLS compared with in OAFLS. miR‑34a‑3p overexpression significantly inhibited the proliferation of FLS (P<0.01) by suppressing the expression levels of cyclin‑dependent kinase 2, cell division cycle 25A and cyclin D1 (P<0.01), and arresting FLS cell cycle progression at the G1 phase. Furthermore, the expression levels of MMP‑1 and 9 were markedly decreased, as were the mRNA and protein expression levels of pro‑inflammatory cytokines (tumor necrosis factor α and interleukin 6; P<0.01). Murine double minute 4 (MDM4) was predicted and verified as a potential target gene of miR‑34a‑3p; the 547‑554 nt position of the MDM4 3'‑untranslated region harbored one potential binding site for miR‑204‑3p. The results of the present study indicated that miR‑34a‑3p may be considered a promising therapeutic target for RA through inhibiting FLS proliferation and suppressing the production of pro‑inflammatory cytokines and MMPs.

/pdf/microrna-34a-3p-inhibits-proliferation-of-rheumatoid-iwej4m142x.pdf

MicroRNA‑34a‑3p inhibits proliferation of rheumatoid arthritis fibroblast‑like synoviocytes

Rheumatoid arthritis (RA) is one of the most common autoimmune diseases that affect synovitis, bone, cartilage, and joint. RA leads to bone and cartilage damage and extra-articular disorders. However, the pathogenesis of RA is still unclear, and the lack of effective early diagnosis and treatment causes severe disability, and ultimately, early death. Accumulating evidence revealed that the regulatory network that includes long non-coding RNAs (lncRNAs)/circular RNAs (circRNAs), micro RNAs (miRNAs), and messenger RNAs (mRNA) plays important roles in regulating the pathological and physiological processes in RA. lncRNAs/circRNAs act as the miRNA sponge and competitively bind to miRNA to regulate the expression mRNA in synovial tissue, FLS, and PBMC, participate in the regulation of proliferation, apoptosis, invasion, and inflammatory response. Thereby providing new strategies for its diagnosis and treatment. In this review, we comprehensively summarized the regulatory mechanisms of lncRNA/circRNA-miRNA-mRNA network and the potential roles of non-coding RNAs as biomarkers and therapeutic targets for the diagnosis and treatment of RA.

/pdf/functional-interactions-between-lncrnas-circrnas-and-mirnas-5dq4jeox.pdf

Functional Interactions Between lncRNAs/circRNAs and miRNAs: Insights Into Rheumatoid Arthritis

Osteosarcoma is a most common bone malignant tumor which threatens children and adolescents. Circular RNAs (circRNAs) fundamentally play essential roles in the progress and development of human cancers by sponging with microRNAs (miRNAs). However, the role of circRNAs in osteosarcoma is not clear. The aim of the study was to investigate the roles and molecular mechanism of circRNAs in osteosarcoma. The data from qRT-PCR showed that circ_0051079 expression was higher in osteosarcoma cells and tissues compared to their normal controls. Meanwhile, bioinformatic analysis indicated that circ_0051079 was a sponge of miR-26a-5p, which was verified by luciferase activity assay. Subsequently, TGF-β1 was verified as a putative target mRNA of miR-26a-5p by luciferase assay. Cellular function assays were conducted and the findings revealed that circ_0051079/miR-26a-5p/TGF-β1 regulated osteosarcoma proliferation and metastasis. The study demonstrated that circ_0051079 could act as an oncogene via regulating miR-26a-5p/TGF-β1 and a potential biomarker for osteosarcoma diagnose.

/pdf/hsa-circ-0051079-functions-as-an-oncogene-by-regulating-mir-aps7c9bz27.pdf

Hsa_circ_0051079 functions as an oncogene by regulating miR-26a-5p/TGF-β1 in osteosarcoma.

This paper is being retracted based on publishers' legal criteria. We have received notification from the author, Yonghui Shen, that he had added Dr. Wei Zhang (the first author) as a co-author fraudulently, without his permission or authorization, and that he falsified the confirmation from Dr. Zhang. Dr. Wei Zhang had no contribution to this paper.

/pdf/retracted-mir-26a-5p-regulates-synovial-fibroblast-invasion-1lw7tg3ukv.pdf

Retracted: miR-26a-5p Regulates Synovial Fibroblast Invasion in Patients with Rheumatoid Arthritis by Targeting Smad.

BACKGROUND We studied the expression and effect of miR-26a-5p in synovial fibroblast in patients with rheumatoid arthritis (RA). MATERIAL AND METHODS The synovial tissues of 55 RA patients with total knee arthroplasty performed from January 2016 to December 2016 were collected as the RA group, and 62 patients without RA history amputation or total knee arthroplasty served as the control group. The expressions of miR-26a-5p and Smad 1 mRNA in synovial fibroblast in patients with RA were detected by qPCR; The expression of Smad 1 and TGF-β1 protein in synovial tissue or synovial fibroblasts was detected by immunoblotting. Transwell assay was used to detect the invasive ability of synovial fibroblasts. RESULTS The expression of miR-26a-5p and Smad 1 in synovial fibroblast in patients with RA were significantly higher than those in the control group (P<0.05). The expression of miR-26a-5p in synovial tissue of RA patients was positively correlated with the expression of Smad 1 mRNA (r=0.8982, P<0.001). The luciferase system showed that miR-26a-5p targeting synovial membrane FLS cells (P<0.05); the expression of MMP-1, MMP-3, MMP-13, and TGF-b1 protein and mRNA in the synovial FLS cells of RA patients was significantly decreased; and the expression of miR-26a-5p was significantly decreased in FLS cells with invasive ability. CONCLUSIONS miR-26a-5p is highly expressed in synovial tissue of patients with RA, and its high expression can improve the invasive ability of synovial fibroblasts by targeting Smad 1 gene and accelerating the progression of RA.

miR-26a-5p Regulates Synovial Fibroblast Invasion in Patients with Rheumatoid Arthritis by Targeting Smad 1.

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Retracted: miR-26a-5p Regulates Synovial Fibroblast Invasion in Patients with Rheumatoid Arthritis by Targeting Smad.

miR-26a-5p Regulates Synovial Fibroblast Invasion in Patients with Rheumatoid Arthritis by Targeting Smad 1.