ArticleInternational journal of medical sciences2026
CXCL14 promotes osteosarcoma cell migration and invasion by inducing epithelial-to-mesenchymal transition.
Article in International journal of medical sciences, 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
Osteosarcoma, an aggressive malignancy of long bones in children and young adults, responds poorly to conventional chemotherapy, and distant metastasis remains the principal cause of death. Here we identify chemokine CXCL14 as a driver of epithelial-to-mesenchymal transition (EMT) and metastatic behavior. CXCL14 expression was markedly higher in osteosarcoma cells than in normal osteoblasts. Knockdown of CXCL14 significantly reduced cell migration and wound closure, accompanied by a shift from spindle-like to cobblestone morphology and restoration of epithelial markers. Recombinant CXCL14 promoted EMT with dose-dependent effects. Western blotting showed CXCL14 suppressed E-cadherin while elevating N-cadherin and vimentin, consistent with EMT induction. Pharmacologic and genetic inhibition revealed that PI3K/AKT, MAPK, and NF-κB signaling cascades mediate CXCL14-driven EMT. In an orthotopic mouse model, silencing CXCL14 retarded tumor growth and reduced mesenchymal marker expression
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