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Simvastatin treatment of breast cancer patients led to increased apoptosis and decreased proliferation in tumor samples. Simvastatin deactivated the PI3K/Akt/mTOR and MAPK/ERK pathways by increasing PTEN expression and decreasing phosphorylation of proteins in the pathways such as Akt, S6RP, c-Raf, and ERK1/2. In breast cancer cell lines, simvastatin consistently induced apoptosis and inhibited proliferation in a dose-dependent manner by modulating proteins involved in caspase cascades and cell cycle regula

Author

AYU

Language

EN