ArticleFrontiers in cell and developmental biology2026
Granzyme B knockdown suppresses cell proliferation, migration and invasion of fibroblast-like synoviocytes in rheumatoid arthritis.
Article in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by progressive synovial inflammation, cartilage and bone destruction. Although granzyme B (GZMB) can prevent osteocartilaginous destruction and promote bone formation, its effects and molecular mechanisms in RA remain unclear. We therefore explored the effects of GZMB on RA development at the cellular level. Methods: We analyzed the effects of GZMB on MH7A cell proliferation using Cell Counting Kit-8 assays. Migration and invasion were detected using wound healing and Transwell® assays, respectively, and the cell cycle and apoptosis were assessed using flow cytometry. Additionally, 24 Sprague-Dawley (SD) rats were divided into sham, RA, and RA + GZMB inhibitor groups. Pathological changes, inflammatory factors, and related proteins were assessed in each group after treatment. Furthermore, we evaluated correlations between GZMB and the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway. Results: Granzyme B suppressed cell proliferation, migration and invasion Conclusion: Our findings suggest that GZMB knockdown suppresses cell proliferation, migration and invasion of fibroblast-like synoviocytes in rheumatoid arthritis, and alleviates the progression of RA rats. This therapeutic mechanism may involve regulation of the PI3K/AKT pathway.
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