Exploring Cytotoxic and Apoptotic Effects of Rosuvastatin on Lung Cancer Cell Line

Objective: This study aimed to investigate the efficacy of Rosuvastatin (Ros) in inhibiting lung cancer cell proliferation in compared to standard treatment, doxorubicin (Dox). Methods: A549 cells were divided into four groups (untreated (control), Dox-treated, and Ros-treated cells) and subjected to six concentrations of the tested drugs. After 72 hours, the cytotoxicity and IC50 concentrations of each drug were determined. A549 cells were then subjected to the IC50 concentrations of either Ros or Dox or left untreated.The cell pellets were tested for caspase 3. Acridine orange/ ethidium bromide stain was used to visualize and calculate apoptotic cells. Results: Our results indicated that Ros treatment caused a significant decline in percentage of cellular growth when compared to control group with an IC50 of 45.24 mu g/ml. While for Dox treated cells, only the highest concentration produced a significant reduction in percentage of cellular growth compared to control, with an estimated IC50 of 294.2 mu g/ml. Furthermore, Ros caused a significant elevation in caspase 3 level compared to control. The same effect was nearly observed in Dox-treated cells with no significant difference between them. Additionally, cells treated with Ros exerted a higher percentage ofapoptosis compared to control. For Dox treated cells, the percentage ofapoptosis was lower than that of Ros, however; this effect was statistically non-significant. Conclusion: Our findings confirmed that rosuvastatin suppressed the growth of lung cancer cells by triggering apoptosis via a caspase 3 dependent mechanism.