Oxycodone modulates VEGFA to inhibit cervical cancer cell migration and angiogenesis

Background: Cervical cancer (CC) is a leading cause of cancer-related deaths among women worldwide, necessitating the development of novel therapeutic strategies. Oxycodone, a semi-synthetic opioid, is primarily known for its analgesic properties but has shown potential anti-cancer effects in various malignancies. However, its impact on cervical cancer cells and the underlying mechanisms remain unclear. Methods: Human cervical cancer cell lines Hela and Siha were treated with varying concentrations of oxycodone (10, 20, 40 μg/mL). Cell proliferation was assessed using Cell Counting Kit-8 (CCK-8) and clonogenic assays. Apoptosis was measured by flow cytometry. Cell migration and angiogenesis were evaluated using wound healing and tube formation assays, respectively. VEGFA expression was analyzed by Western blotting. Results: Oxycodone inhibited the proliferation of cervical cancer cells. It induced apoptosis in cervical cancer cells. Oxycodone suppressed the migration and angiogenesis of cervical cancer cells. Mechanistically, oxycodone regulated vascular endothelial growth factor A (VEGFA) expression, leading to the inhibition of cell migration and angiogenesis. Conclusions: Oxycodone exhibits significant anti-cancer effects on cervical cancer cells by inhibiting proliferation, inducing apoptosis, and suppressing migration and angiogenesis through the regulation of VEGFA expression. These findings suggest that oxycodone has potential as a therapeutic agent for cervical cancer treatment.