Modulatory effect of α-Bisabolol on induced apoptosis via mitochondrial and NF-κB/Akt/PI3K Signaling pathways in MCF-7 breast cancer cells

Abstract

Abstract Breast cancer is a highly feared form of cancer that predominantly affects women. In pursuing effective treatments, herbal medicine has garnered attention as a viable resource. It holds promise as an alternative approach for managing and combating breast cancer. The primary objective of the research was to explore how α-Bisabolol hinders the growth of MCF-7 human breast cancer cells and decipher its molecular mechanisms of reducing cell proliferation and promoting apoptosis. In the experiment, cultured MCF-7 cells were divided into four distinct groups: The first group functioned as the control, whereas the second, third, and fourth groups received separate treatments of α-Bisabolol at varying concentrations. After allowing the cells to incubate for a 24-hour, we examined them to assess any alterations in their morphology after applying α-Bisabolol. This treatment led to the suppression of cell growth, an elevation in the generation of reactive oxygen species (ROS) and the initiation of apoptosis. Furthermore, examination through western blot and real-time PCR unveiled that cell treated with α-Bisabolol exhibited reduced levels of the cell survival gene Bcl-2, alongside elevated levels of the pro-apoptotic genes Bax, Bad, Caspase-3, Caspase-9, and cytochrome c. Meanwhile, NF-κB, p-PI3K, and p-Akt proteins were downregulated in α-Bisabolol treated cells. These results suggest that α-Bisabolol diminishes the cell viability of MCF-7 cells and triggers cellular apoptosis through both the mitochondrial pathway and the NF-κB/Akt/PI3K signaling pathways.