ArticleInternational journal of molecular sciences2021
14-3-3η Promotes Invadosome Formation via the FOXO3-Snail Axis in Rheumatoid Arthritis Fibroblast-like Synoviocytes.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Hydrogels as Local Structural-Protective Platforms in Rheumatoid Arthritis: An Evidence-Graded Review Across the Synovium-Cartilage-Bone Axis.Gels (Basel, Switzerland) · 2026Review
- Vascular endothelial growth factor (VEGF) biology and its proposed role in rheumatic diseases pathogenesis.Advances in rheumatology (London, England) · 2026Article
- Genetic analysis of Behçet's disease using whole-exome sequencing and bioinformatics analysis in Korean patients.Frontiers in genetics · 2026Article
- MDMX reprograms glycolysis of hepatocellular carcinoma via 14-3-3γ/FOXO1.Cell death discovery · 2025Article
- Understanding the role of 14-3-3Ƞ protein in rheumatoid arthritis: from molecular dysregulation to therapeutic Redirection.Molecular biology reports · 2025Review
- ARRB2 promotes cervical cancer progression via stabilizing CDC25A mRNA through m6A-IGF2BP1-dependent manner.NPJ precision oncology · 2025Article
- Versatility of 14-3-3 proteins and their roles in bone and joint-related diseases.Bone research · 2024Review
- Toripalimab, a therapeutic monoclonal anti-PD-1 antibody with high binding affinity to PD-1 and enhanced potency to activate human T cells.Cancer immunology, immunotherapy : CII · 2024Article
- Serum 14‑3‑3η levels are increased and associated with a higher risk of osteoporosis in patients with rheumatoid arthritis: A meta‑analysis.Experimental and therapeutic medicine · 2024Article
- The Pathogenesis of Rheumatoid Arthritis Breakthroughs in Molecular Mechanisms 1 and 2.International journal of molecular sciences · 2023Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Erosive destruction of joint structures is a critical event in the progression of rheumatoid arthritis (RA), in which fibroblast-like synoviocytes (FLS) are the primary effectors. We previously reported that the ability of RA FLS to degrade extracellular matrix (ECM) components depends on the formation of actin-rich membrane protrusions, called invadosomes, through processes that remain elusive. 14-3-3η belongs to a family of scaffolding proteins involved in a wide range of cellular functions, and its expression is closely related to joint damage and disease activity in RA patients. In this study, we sought to assess the role of 14-3-3η in joint damage by examining its contribution to the invadosome formation phenotype of FLS. Using human primary FLS, we show that 14-3-3η expression is closely associated with their ability to form invadosomes. Furthermore, knockdown of 14-3-3η using shRNAs decreases the level of invadosome formation in RA FLS, whereas addition of the recombinant protein to FLS from healthy individuals promotes their formation. Mechanistic studies suggest that 14-3-3η regulates invadosome formation by increasing Snail expression, a mechanism that involves nuclear exclusion of the transcription repressor FOXO3. Our results implicate the 14-3-3η-FOXO3-Snail axis in promoting the aggressive ECM-degrading phenotype of RA FLS, and suggest a role for this scaffolding protein in cartilage degradation.
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