ArticleImmunity, inflammation and disease2022
KLF9 positively regulates TRIM33 to inhibit abnormal synovial fibroblast proliferation, migration as well as inflammation in rheumatoid arthritis.
Article in Immunity, inflammation and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Dysregulation of the KLF9/TXNRD2 Axis Leads to Mitochondrial DNA Oxidation and NLRP3 Inflammasome Activation in Ulcerative Colitis.Journal of biochemical and molecular toxicology · 2026Article
- TRIM proteins as emerging regulators of immune pathways: potential therapeutic targets in immune-related disorders.Frontiers in immunology · 2026Review
- Nuclear binding SET domain 1 alleviates cartilage ferroptosis in knee osteoarthritis by upregulating the krüppel-like factor 9/autophagy-related 14 pathway via H3K36me2 modification.Journal of cell communication and signaling · 2025Article
- Aberrant expression of TRIM44, transcriptionally regulated by KLF9, contributes to the process of diabetic retinopathy.Journal of translational medicine · 2025Article
- KLF9, Epigenetic Silenced by DNMT1, Promotes ERK-Mediated Ferroptosis of Osteoarthritic Chondrocytes Through Transcriptionally Regulating CYP1B1.Journal of cellular and molecular medicine · 2025Article
- KLF transcription factors in bone diseases.Journal of cellular and molecular medicine · 2024Review
- Mechanism of KLF9 in airway inflammation in chronic obstructive pulmonary.Immunity, inflammation and disease · 2023Article
- KLF9 positively regulates TRIM33 to inhibit abnormal synovial fibroblast proliferation, migration as well as inflammation in rheumatoid arthritis.Immunity, inflammation and disease · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRheumatoid arthritis (RA) can cause irreversible joint injury and serious disability. This study aimed to investigate how TRIM33 regulated by KLF9 affects the aggressive behaviors of synovial fibroblasts induced by tumor necrosis factor-α (TNF-α). MATERIALS AND
methodsTNF-α-induced MH7A cells were used to simulate the in vitro model of RA. TRIM33 and KLF9 expression in TNF-α-challenged MH7A cells and transfection efficiency were analyzed via real-time reverse transcription polymerase chain reaction together with western blot. The viability, proliferation, invasion, and migration of TNF-α-induced MH7A cells after transfection was respectively detected by CCK-8, EdU staining, transwell, and wound-healing assays. The expression of invasion and migration-related proteins and inflammation-related proteins was determined by western blot and the levels of inflammatory factors were detected by enzyme-linked immunosorbent assay. The combination between TRIM33 and KLF9 was substantiated through dual-luciferase reporter assay and chromatin immunoprecipitation.
resultsTRIM33 and KLF9 expression in TNF-α-challenged MH7A cells was downregulated. TRIM33 elevation inhibited TNF-α-elicited proliferation, metastasis as well as inflammation of MH7A cells. Moreover, KLF9 was combined with TRIM33 and KLF9 promoted transcription of TRIM33. The inhibitory effect of TRIM33 overexpression on proliferation, invasion and migration and inflammation of MH7A cells induced by TNF-α was alleviated by the downregulation of KLF9.
conclusionKLF9 positively regulates TRIM33 to suppress the abnormal MH7A cell proliferation, migration, and reduce inflammation upon exposure to TNF-α, which was reversed by inhibiting KLF9.
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