Epigallocatechin-۳-Gallate Induces Apoptosis through Up-regulation of Bax and Down-regulation of Bcl-۲ in Prostate Cancer Cell Line
- سال انتشار: 1395
- محل انتشار: مجله بین المللی آزمایشگاه پزشکی، دوره: 3، شماره: 4
- کد COI اختصاصی: JR_JIML-3-4_006
- زبان مقاله: انگلیسی
- تعداد مشاهده: 72
نویسندگان
۱Department of Reproductive Biology, Faculty of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran. ۲Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Department of Biochemistry and Clinical Laboratories, Faculty of Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
Department of Laboratory Medicine, Faculty of Paramedical Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
۳Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. ۴Department of Biochemistry and Clinical Laboratories, Faculty of Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.
چکیده
Background and Aims: Epigallocatechin-۳-gallate (EGCG) is a polyphenolic compound from green tea, which its anticancer effects on many types of cancers have been confirmed, but the molecular mechanism by which EGCG induces apoptosis remains unknown. The aim of the present study was to investigate anti-proliferative properties and apoptotic signaling pathway of EGCG on PC۳ human prostate cancer cells. Materials and Methods: Cytotoxic effect of EGCG on prostate cancer cell line (PC۳) was evaluated by MTT assay. DAPI staining was carried out to determine the morphological appearance of cells. Finally, the expression of Bax and Bcl-۲ (apoptosis-regulating genes) were evaluated by quantitative Real-time polymerase chain reaction (PCR). Results: Cytotoxicity evaluations demonstrated that EGCG prevented prostate cancer cells growth in a time and dose depended manner, but the effect of treatment duration is more significant than effect of concentration. Cell growth inhibition was found to be accompanied by nucleus condensation or chromatin fragmentations which are signs of apoptosis, as assessed by DAPI staining. Quantitative Real-time PCR results demonstrated that EGCG causes up-regulation of Bax as a pro-apoptotic protein, and down-regulation of Bcl-۲ as an anti-apoptotic protein, thus shifting the Bax/Bcl-۲ ratio in favor of apoptosis. Conclusions: It is tempting to suggest that consumption of EGCG could be an effective strategy to inhibit prostate cancer. Our results demonstrated that increase in the ratio of Bax/Bcl-۲, is the probable molecular mechanisms through which EGCG induces apoptosis in PC۳ cells.کلیدواژه ها
Apoptosis, Bax, Bcl-۲, EGCG, Prostate cancerاطلاعات بیشتر در مورد COI
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