ArticleInflammation2018
Sam68 Promotes Invasion, Migration, and Proliferation of Fibroblast-like Synoviocytes by Enhancing the NF-κB/P65 Pathway in Rheumatoid Arthritis.
Article in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Targeting RNA binding proteins with small-molecule inhibitors: Advances, challenges, and therapeutic opportunities.Acta pharmaceutica Sinica. B · 2026Review
- Identification of Hepatocellular Carcinoma Subtypes Based on Global Gene Expression Profiling to Predict the Prognosis and Potential Therapeutic Drugs.Biomedicines · 2025Article
- Recent Progress in the Research on RNA-Binding Proteins in Bone Development and Diseases.International journal of molecular sciences · 2024Review
- Role of Sam68 as an adaptor protein in inflammatory signaling.Cellular and molecular life sciences : CMLS · 2024Review
- New advances in genomics and epigenetics in antiphospholipid syndrome.Rheumatology (Oxford, England) · 2024Review
- KHDRBS1 as a novel prognostic signaling biomarker influencing hepatocellular carcinoma cell proliferation, migration, immune microenvironment, and drug sensitivity.Frontiers in immunology · 2024Article
- Article
- Splicing machinery is impaired in rheumatoid arthritis, associated with disease activity and modulated by anti-TNF therapy.Annals of the rheumatic diseases · 2022Article
- Article
- Sam68 contributes to intestinal inflammation in experimental and human colitis.Cellular and molecular life sciences : CMLS · 2021Article
- MLL3 Inhibits Apoptosis of Rheumatoid Arthritis Fibroblast-Like Synoviocytes and Promotes Secretion of Inflammatory Factors by Activating CCL2 and the NF-κB Pathway.Inflammation · 2021Article
- miR-200b-3p alleviates TNF-α-induced apoptosis and inflammation of intestinal epithelial cells and ulcerative colitis progression in rats via negatively regulating KHDRBS1.Cytotechnology · 2021Article
- NEAT1 promotes the repair of abdominal aortic aneurysms of endothelial progenitor cells via regulating miR-204-5p/Ang-1.American journal of translational research · 2021Article
- METTL3 Promotes Activation and Inflammation of FLSs Through the NF-κB Signaling Pathway in Rheumatoid Arthritis.Frontiers in medicine · 2021Article
- Induced, but not natural, regulatory T cells retain phenotype and function following exposure to inflamed synovial fibroblasts.Science advances · 2020Article
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- Sam68 impedes the recovery of arterial injury by augmenting inflammatory response.Journal of molecular and cellular cardiology · 2019Article
- Sam68 mediates high glucose‑induced podocyte apoptosis through modulation of Bax/Bcl‑2.Molecular medicine reports · 2019Article
- Losartan suppresses the inflammatory response in collagen-induced arthritis by inhibiting the MAPK and NF-κB pathways in B and T cells.Inflammopharmacology · 2019Article
Corrections and comments
- Erratum issuedCorrection to: Sam68 Promotes Invasion, Migration, and Proliferation of Fibroblast-like Synoviocytes by Enhancing the NF-κB/P65 Pathway in Rheumatoid Arthritis.2019 · Qin, Rongqin [corrected to Qin, Rongqing]
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Src-associated substrate during mitosis of 68 KDa (Sam68), also known as KH domain containing, RNA binding, signal transduction associated 1 (KHDRBS1), is the prototypic member of the signal transduction activator of RNA (STAR) family of RNA-binding proteins. Previous studies have indicated that Sam68 regulates nuclear transcription factor kappa B (NF-κB) to mediate inflammation. In this study, we analyzed the effect and possible mechanisms of Sam68 in rheumatoid arthritis (RA). By western blot analysis and immunohistochemistry, we found that the expression of Sam68 in synovial tissue of RA patients was increased compared with the control group. Immunoflourescent staining demonstrated that Sam68 co-localized with fibroblast-like synoviocytes (FLS) of RA patients. Additionally, the expression of Sam68 in FLS was increased by tumor necrosis factor (TNF)-α stimulation, in a time-dependent manner. Upon TNF-α treatment, Sam68 translocated from the cytoplasm to the nucleus where it interacted with the p65 subunit of NF-κB, as examined by immunoprecipitation and immunofluorescent staining assay. Furthermore, inhibiting the expression of Sam68 by siRNA significantly suppressed the TNF-α-induced expression of interleukin (IL)-6, and matrix metalloproteinase (MMP)-1, reduced the proliferation, migration, and invasion, and markedly decreased the phosphorylation of P65 and IκBα in FLS. Collectively, our findings suggested that Sam68 contributed to the production of inflammatory cytokines, proliferation, migration, and invasion of RA FLS through the NF-κB P65 signal transduction pathway and underscored the importance of Sam68 in the inflammation process of RA.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.