Coronin-1A Modulates Oscc Immune Microenvironment Via Cytoskeleton-Mitochondria Interaction

Oral squamous cell carcinoma (OSCC) is a prevalent malignancy with poor prognosis due to its invasiveness and high recurrence rates. The role of Coronin-1a, a cytoskeletal regulator, in OSCC progression and immune modulation is unclear. This study investigates Coronin-1a as a potential tumor suppressor in OSCC, focusing on its effects on cytoskeletal dynamics, mitochondrial integrity, and immunogenic cell death (ICD). RNA-seq and bioinformatics analyses evaluated Coronin-1a expression in OSCC. qRT-PCR and Western Blot detected Coronin-1a expression in tissues and cells. Coronin-1a overexpression and knockdown cell models were established, and biological functions were examined using proliferation, apoptosis, and migration assays. Immunofluorescence staining investigated Coronin-1a localization and its effects on cytoskeleton and mitochondrial morphology. qRT-PCR verified the mechanisms of Coronin-1a in ICD regulation. Coronin-1a expression was upregulated in OSCC tissues, correlating with better 5-year survival rates. High Coronin-1a expression was associated with increased CD4+ and CD8+ T cell infiltration. Experiments showed that Coronin-1a inhibited cell proliferation and migration, promoted apoptosis, and altered cytoskeleton and mitochondrial morphology, with increased mtDNA release. RNA-seq identified 30 significantly altered immune-related genes in Coronin-1a-overexpressing cells, enriched in apoptosis pathways. qRT-PCR confirmed upregulation of ICD markers calreticulin (CALR) and CXCL10. Coronin-1a may promote apoptosis and ICD in OSCC by modulating cytoskeleton-mitochondria interactions and mtDNA release, contributing to improved survival. These findings provide a theoretical basis for developing new immunotherapeutic strategies for OSCC.