Atorvastatin can inhibit ovarian cancer by decreasing VEGF, TGF-β1 and increasing cytochrome-c and caspase-3 expressions

Abstract

Objective: Atorvastatin (ATV), being widely utilized in clinical practice, is recognized as a prevalent cancer drug with established safety profiles. The objective of this study was to examine the potential anti-tumor effects of ATV in ovarian cancer (OC), as well as explore its underlying mechanism. Methods: The CCK-8 method was employed to assess the efficacy of ATV on both OC cells and normal ovarian epithelial cells. Furthermore, the anti-proliferative impact of ATV on OC cells was determined through CCK-8 and colony formation techniques. Additionally, flow cytometry was employed to detect apoptosis in SKOV3 cells, while Transwell assays were utilized to assess cell migration and invasion. Western Blot analysis was conducted to evaluate EMT-related proteins (E-cadherin, Vimentin, and N-cadherin), as well as VEGF, TGF-β1, cytochrome-c, and caspase-3. Result: ATV had dose-dependent and time-dependent anti-tumor activity on SKOV3 cells, which promoted apoptosis of tumor cells, significantly up-regulated E-cadherin, cytochrome-c, and caspase3, and downregulated Vimentin, N-cadherin, VEGF, and TGF-β1. Conclusion: ATV exhibits anti-tumor properties on SKOV3 cells by modulating various cellular factors, including reducing VEGF and TGF-β1 levels, enhancing cytochrome-c and caspase-3 expression, and inhibiting tumor invasion and metastasis. The findings of this study contribute to the establishment of a scientific foundation for the potential clinical utilization of ATV in the management of OC.