ArticleCancer cell international2025
STIM1 signaling modulates invasive phenotypic plasticity by regulating calpain-dependent cleavage of integrin-β4 in nasopharyngeal carcinoma cells.
Article in Cancer cell international, 2025. 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
backgroundStromal interaction molecule 1 (STIM1)-mediated Ca
methodsWestern blotting of epithelial and mesenchymal markers, cell migration and colony formation assays were performed to evaluate the EGF-stimulated EMT and laminin-induced MET in vitro. A zebrafish xenograft model was employed to elucidate the proliferation of transplanted NPC cell spheroids in vivo. A tail vein injection-lung metastasis mouse model was utilized to determine the capacity for distant metastatic colonization of NPC cells. Immunohistochemical analysis was conducted to detect the expression level of integrin-β4 in NPC tissues.
resultsIntegrin-β4 was required for the bi-directional epithelial-mesenchymal transition in NPC cells. Silencing of integrin-β4 inhibited cell migration and clonogenicity in vitro, reduced clonal expansion of tumor cell clusters in zebrafishes, and eliminated distant metastatic colonization in mice. STIM1 Ca
conclusionSTIM1 signaling promotes invasiveness by enabling accelerated subcellular integrin-β4 redistribution, which is essential for maintaining the invasive plasticity of NPC cells.
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