The mechanism of CAV1 in cervical cancer

Objective To investigate the expression level, clinical significance, and molecular mechanism of caveolin-1 (CAV1) in cervical cancer. Methods Tissue microarrays and immunohistochemistry were used to detect CAV1 expression in cervical cancer and adjacent tissues. A stable CAV1-overexpressing HeLa cell model was established. Cell proliferation, migration, and invasion were assessed via CCK-8, scratch, and Transwell assays. qRT-PCR and Western blot were performed to examine downstream genes EHD2 and FSCN1. TCGA database and bioinformatics analyses (functional enrichment, immune infiltration) were also conducted. Results CAV1 expression was significantly lower in cervical cancer tissues compared to adjacent normal tissues. Overexpression of CAV1 markedly inhibited HeLa cell proliferation, migration, and invasion, and downregulated EHD2 and FSCN1 expression at both mRNA and protein levels. Bioinformatics analysis confirmed low CAV1 expression in cervical cancer, associated with poor prognosis, cell proliferation, adhesion, cytoskeleton remodeling, and immune microenvironment. Conclusion CAV1 is downregulated in cervical cancer and acts as a tumor suppressor, likely through inhibition of EHD2 and FSCN1. CAV1 and its downstream pathways represent potential therapeutic targets.