Carboxyamido-triazole inhibits proliferation of human breast cancer cells via G2/M cell cycle arrest and apoptosis

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Abstract

Carboxyamido-triazole (CAI), a voltage-independent calcium channel inhibitor, has been shown to be able to induce growth inhibition and apoptosis in cancer cells. In the present study, we demonstrate that CAI significantly inhibits proliferation of cultured MCF-7 human breast cancer cells in a dose-dependent manner with an IC50 of ˜ 26 μM. Reduced proliferation of MCF-7 cells in the presence of CAI correlated with accumulation of cells in G2/M phase and induction of apoptosis. A treatment of MCF-7 cells with 30 μM CAI caused a time-dependent decrease in the levels of proteins that regulate G2/M progression, including Cdk1, Cyclin B1, and Cdc25C. A simultaneous increase in the expression of p21 protein was observed. We also demonstrated a concurrent decrease of the mitochondrial membrane potential (ΔΨm), and down-regulation of anti-apoptotic protein Bcl-2. In conclusion, it seems reasonable to hypothesize that the antitumor effect of CAI in MCF-7 cells is based on G2/M cell cycle arrest and inducing apoptosis.

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