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Thymoquinone induces apoptosis via targeting the Bax/BAD and Bcl-2 pathway in breast cancer cells

Yıl 2019, Cilt: 46 Sayı: 3, 411 - 417, 16.09.2019
https://doi.org/10.5798/dicletip.620329

Öz

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. 

Kaynakça

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Toplam 29 adet kaynakça vardır.

Ayrıntılar

Birincil Dil İngilizce
Konular Sağlık Kurumları Yönetimi
Bölüm Original Articles
Yazarlar

İbrahim Halil Yıldırım 0000-0001-5518-5004

Ali Ahmed Azzawri Bu kişi benim 0000-0001-5311-8887

Tuğçe Duran Bu kişi benim 0000-0002-7353-4527

Yayımlanma Tarihi 16 Eylül 2019
Gönderilme Tarihi 24 Aralık 2018
Yayımlandığı Sayı Yıl 2019 Cilt: 46 Sayı: 3

Kaynak Göster

APA Yıldırım, İ. H., Azzawri, A. A., & Duran, T. (2019). Thymoquinone induces apoptosis via targeting the Bax/BAD and Bcl-2 pathway in breast cancer cells. Dicle Medical Journal, 46(3), 411-417. https://doi.org/10.5798/dicletip.620329
AMA Yıldırım İH, Azzawri AA, Duran T. Thymoquinone induces apoptosis via targeting the Bax/BAD and Bcl-2 pathway in breast cancer cells. diclemedj. Eylül 2019;46(3):411-417. doi:10.5798/dicletip.620329
Chicago Yıldırım, İbrahim Halil, Ali Ahmed Azzawri, ve Tuğçe Duran. “Thymoquinone Induces Apoptosis via Targeting the Bax/BAD and Bcl-2 Pathway in Breast Cancer Cells”. Dicle Medical Journal 46, sy. 3 (Eylül 2019): 411-17. https://doi.org/10.5798/dicletip.620329.
EndNote Yıldırım İH, Azzawri AA, Duran T (01 Eylül 2019) Thymoquinone induces apoptosis via targeting the Bax/BAD and Bcl-2 pathway in breast cancer cells. Dicle Medical Journal 46 3 411–417.
IEEE İ. H. Yıldırım, A. A. Azzawri, ve T. Duran, “Thymoquinone induces apoptosis via targeting the Bax/BAD and Bcl-2 pathway in breast cancer cells”, diclemedj, c. 46, sy. 3, ss. 411–417, 2019, doi: 10.5798/dicletip.620329.
ISNAD Yıldırım, İbrahim Halil vd. “Thymoquinone Induces Apoptosis via Targeting the Bax/BAD and Bcl-2 Pathway in Breast Cancer Cells”. Dicle Medical Journal 46/3 (Eylül 2019), 411-417. https://doi.org/10.5798/dicletip.620329.
JAMA Yıldırım İH, Azzawri AA, Duran T. Thymoquinone induces apoptosis via targeting the Bax/BAD and Bcl-2 pathway in breast cancer cells. diclemedj. 2019;46:411–417.
MLA Yıldırım, İbrahim Halil vd. “Thymoquinone Induces Apoptosis via Targeting the Bax/BAD and Bcl-2 Pathway in Breast Cancer Cells”. Dicle Medical Journal, c. 46, sy. 3, 2019, ss. 411-7, doi:10.5798/dicletip.620329.
Vancouver Yıldırım İH, Azzawri AA, Duran T. Thymoquinone induces apoptosis via targeting the Bax/BAD and Bcl-2 pathway in breast cancer cells. diclemedj. 2019;46(3):411-7.