[01] Rozina Akter, Department of Applied Biosciences, University of Arkansas at Little Rock, Little Rock, Arkansas, USA. [02] Michael A. Gealt, Central Michigan University, Mount Pleasant, Michigan, USA. [03] Maurice G. Kleve, Department of Biology, University of Arkansas at Little Rock, Little Rock, Arkansas, USA. [04] Md. Zakir Hossain, Department of Pharmaceutical Sciences, Biomanufacturing Research Institute and Technology Enterprise (BRITE), North Carolina Central University, Durham, North Carolina, USA.

The present study aimed to explore the molecular mechanisms and biological pathways involved in Wortmannin induced breast cancer MCF-7 programmed cell death. The direct cellular and molecular effect of Wtmn was investigated selectively on the MCF-7 cancer cell line. To study morphological effects phase contrast microscopy was used. The mitochondrial membrane potential and detection of caspase activity were investigated using fluorescent microscopy. Our morphological, molecular, and caspases expression indicated the intrinsic apoptosis pathways involved, and confirmed the role of Wtmn in these pathways. Our experimental results demonstrated that Wortmannin (Wtmn), an irreversible and selective PI3-K inhibitor, inhibits the proliferation of MCF-7 breast cancer cells, and facilitates their entry into apoptosis. Our data established the anti-cancer properties of Wtmn on MCF-7 breast cancer cells. These studies directed us towards elucidating the molecular mechanisms and biological pathways mainly involved in this process. This findings offer potential drug screening to search for novel inducers of apoptosis on MCF-7 cells, and could be used to design better drugs.

MCF-7, Wortmannin, Caspase, Mitochondrial Membrane Potential, and Apoptosis

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