Inhibition of PTK6 Hinders the Growth and Migration of Ovarian Cancer and Its Potential Clinical Significance

Background This study investigates the oncogenic role of Protein Tyrosine Kinase 6 (PTK6) in ovarian cancer (OC), focusing on its clinical prognosis, and its function on OC. Methods Multi-omics analyses to identify differentially expressed genes (DEGs). PTK6 expression was validated across datasets and correlated with survival, tumor stage and signaling pathways. Functional assays included lentiviral PTK6 knockdown and pharmacological inhibition (tilfrinib) in OC cells, evaluated via CCK-8, EdU, wound healing assay, colony formation, and molecular docking. Results PTK6 was upregulated in OC, with high expression linked to poor overall, disease-specific, and progression-free survival. Single-cell analysis localized PTK6 predominantly to epithelial and malignant cells. PTK6 knockdown suppressed the proliferation and migration of Caov-4 and ID8 cells. Tilfrinib forms a stable complex with PTK6 and inhibits cell proliferation in a dose-dependent manner. Conclusions PTK6 drives OC progression via proliferation, immune evasion, and oncogenic pathway regulation. Inhibition of PTK6 by tilfrinib constitutes a promising targeted therapy for ovarian cancer.