Simvastatin potently induces calcium-dependent apoptosis of human leiomyoma cells
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Updated: Apr 21, 2026
Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
Mostafa A Borahay1, Gokhan S Kilic2, Chandrasekha Yallampalli3
1From the Department of Obstetrics and Gynecology, University of Texas Medical Branch, Galveston, Texas 77555, the Department of Biochemistry and Molecular Biology, University of Texas Health Sciences Center at Houston, Houston, Texas 77030, maboraha@utmb.edu.
Abstract:
Statins are drugs commonly used for the treatment of high plasma cholesterol levels. Beyond these well known lipid-lowering properties, they possess broad-reaching effects in vivo, including antitumor effects. Statins inhibit the growth of multiple tumors. However, the mechanisms remain incompletely understood. Here we show that simvastatin inhibits the proliferation of human leiomyoma cells. This was associated with decreased mitogen-activated protein kinase signaling and multiple changes in cell cycle progression. Simvastatin potently stimulated leiomyoma cell apoptosis in a manner mechanistically dependent upon apoptotic calcium release from voltage-gated calcium channels. Therefore, simvastatin possesses antitumor effects that are dependent upon the apoptotic calcium release machinery.
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