ArticleCellular & molecular biology letters2025
CIP2A promotes inflammation and exacerbates osteoarthritis by targeting CEMIP.
Article in Cellular & molecular biology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Oridonin ameliorates the ferroptosis of chondrocyte to play a chondroprotective role in osteoarthritis.Journal of bioenergetics and biomembranes · 2026Article
- STOML2 Alleviates Osteoarthritis by Regulating Mitochondrial Energy Metabolism and Oxidative Stress.Genetics research · 2026Article
- Gut microbiota-immune crosstalk in osteoarthritis: pathogenic mechanisms and emerging therapeutic opportunities.Frontiers in microbiology · 2026Review
- Downregulation of FTO aggravates osteoarthritis with obesity by erasing mMilitary Medical Research · 2026Article
- CDK5 regulates PPARγ/NF-κB signaling to exacerbate obesity-related osteoarthritis via modulating macrophage polarization and chondrocyte apoptosis.Cellular & molecular biology letters · 2025Article
- The Emerging Role of the Cancerous Inhibitor of Protein Phosphatase 2A in Pulmonary Diseases.Medicina (Kaunas, Lithuania) · 2025Review
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Abstract
backgroundOsteoarthritis (OA) is a chronic joint disease characterized by cartilage degeneration with unclear pathogenic mechanism. This study aims to discuss the regulatory role of cancerous inhibitor of protein phosphatase 2A (CIP2A) in OA pathogenesis and to elucidate the molecular mechanisms.
methodsMouse chondrocytes were induced by interleukin-1β (IL-1β) to mimic OA inflammation, and extracellular matrix (ECM) homeostasis and inflammatory factors were evaluated at mRNA and protein levels. A mouse model of OA was induced by destabilization of medial meniscus (DMM) surgery. Histopathological staining was used to assess the cartilage destruction of human and mouse. Osteophyte formation was observed using micro-computed tomography (CT). Downstream of CIP2A was screened by RNA sequencing and coimmunoprecipitation coupled with mass spectrometry in mouse chondrocytes.
resultsCIP2A was downregulated in cartilage of patients with OA and DMM mouse models, as well as in IL-1β-induced mouse chondrocytes. However, CIP2A overexpression promoted ECM degradation and inflammatory processes and exacerbated cartilage destruction and osteophyte formation. By contrast, knockdown or pharmacological inhibition of CIP2A alleviated cartilage degeneration to a certain extent, with no improvement in osteophytes formation caused by OA. Mechanistically, CIP2A interacted with its downstream cell migration-inducing protein (CEMIP) and activated the nuclear factor kappa B (NF-κB) signaling pathway, resulting in the imbalance of cartilage anabolic and catabolic factors and the activation of inflammation in the development of OA. In addition, CIP2A was ubiquitinated in mouse chondrocytes, causing it to be degraded, which could be a negative feedback of CIP2A expression in OA.
conclusionsCIP2A targets CEMIP to activate NF-κB signaling pathway, which in turn aggravates cartilage destruction and inflammation and ultimately accelerates OA development. Our results suggest the potential role of the CIP2A/CEMIP axis as a therapeutic target for OA.
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