Dicle Medical Journal / Dicle Tip Dergisi · 2019 · 13 citations · 14 references
MedicineOncologyPharmacologyApoptosisCancer PharmacologyMolecular OncologyApoptosis In CancerApoptosis ModulationApoptosis PharmacologyBcl-2 Family ProteinsAnti-apoptotic AgentsAnticancer ActivityApoptosis Signaling In CancerApoptosis TargetingApoptotic Signaling In CancerCancer Cell ApoptosisCancer Cell Proliferation InhibitionPro-apoptotic Bax Activation
Objective: Nigella sativa, commonly known as the black seed, has been used since ancient times in folk medicine, and its various therapeutic benefits have been mentioned in some ancient medical sources and confirmed by modern science. Thymoquinone is the major compound and essential active ingredient of Nigella sativa seed oil. Thymoquinone has been reported to have high biological activity and broad therapeutic potential through several mechanisms that affect cells including anti-oxidant, anti-inflammatory, and anti-tumor properties. Although it has been widely reported that Thymoquinone inhibits cell growth and proliferation and stimulates apoptosis in various types of cancer cells, the mechanisms and signaling pathways are not fully understood. The aim of this study was to determine the effect of Thymoquinone on apoptosis in both tumor and non-tumor cells. Methods: In this study, breast cancer cell line (MCF-7) was used as tumor cells and Human Embryonic Kidney Cell line (HEK293) was used as non-tumor cells. Cells were treated with Thymoquinone and viability test performed by MTT assay.Gene expression of apoptosis markers such as Bax, BAD, Bcl-2, and p53 was determined by Real-Time PCR. HEK293 cells were used as non-tumor control. Results and Conclusion: Results suggest that Thymoquinone has a strong effect on cell proliferation and vitality. Thymoquinone has increased the expression of BAD, Bax genes which induce apoptosis and decreased the p53 gene in breast cancer cells. Therefore Thymoquinone promotes apoptosis and enhances anti-cancer efficacy in breast cancer cells.
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Bad, a heterodimeric partner for Bcl-xL and Bcl-2, displaces bax and promotes cell death
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