DLGAP5 promotes salivary adenoid cystic carcinoma proliferation and metastasis through PI3K/AKT pathway.

To elucidate the oncogenic role of DLGAP5 in salivary adenoid cystic carcinoma (SACC), we characterized its expression patterns and functional impact on malignant phenotypes including proliferation, migration, and invasion; we assessed DLGAP5 expression using the GEO database, examined its effects on SACC cells through DLGAP5 knockdown and overexpression experiments, verified these findings with a nude mouse subcutaneous tumor model, and employed virtual screening to identify the lead compound ZINC3809191 targeting DLGAP5, whose inhibitory effects on SACC were confirmed in vitro. Our results showed that DLGAP5 was highly expressed in SACC and correlated with clinical stage and pathological grade, and it promoted the proliferation, migration, and invasion of SACC cells via the PI3K/AKT signaling pathway; additionally, the lead compound ZINC3809191 demonstrated significant ability to inhibit the proliferation, migration, and invasion of SACC cells. Collectively, our findings indicate that DLGAP5 is upregulated in SACC, associated with clinical stage and pathological grade, and plays a regulatory role in key malignant phenotypes of SACC cells, while the identification of ZINC3809191 with potent anti-tumor activity against DLGAP5 provides a crucial theoretical foundation for the development of potential therapeutic strategies for SACC.