Emodin-Provoked Oxidative Stress Induces Apoptosis in Human Colon Cancer HCT116 Cells through a p53-Mitochondrial Apoptotic Pathway

Xie, Mei-Juan; Ma, Yi-Hua; Miao, Lin; Wang, Yan; Wang, Hai-Zhen; Xing, Ying-Ying; Xi, Tao; Lu, Yuan-Yuan

추천

검색

자료유형: 학술저널

저자정보: Xie, Mei-Juan (State Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University) Ma, Yi-Hua (State Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University) Miao, Lin (State Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University) Wang, Yan (State Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University) Wang, Hai-Zhen (State Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University) Xing, Ying-Ying (State Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University) Xi, Tao (State Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University) Lu, Yuan-Yuan (State Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutical University)

저널정보: 아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제15권 제13호

발행연도: 2014.1

수록면: 5,201 - 5,205 (5page)

이용수

📌

연구주제

📖

연구배경

🔬

연구방법

🏆

연구결과

초록· 키워드

오류제보하기

Emodin, a natural anthraquinone isolated from the traditional Chinese medicine Radix rhizoma Rhei, can induce apoptosis in many kinds of cancer cells. This study demonstrated that emodin induces apoptosis in human colon cancer HCT116 cells by provoking oxidative stress, which subsequently triggers a p53-mitochondrial apoptotic pathway. Emodin induced mitochondrial transmembrane potential loss, increase in Bax and decrease in Bcl-2 expression and mitochondrial translocation and release of cytochrome c to cytosol in HCT116 cells. In response to emodin-treatment, ROS increased rapidly, and subsequently p53 was overexpressed. Pretreatment with the antioxidant NAC diminished apoptosis and p53 overexpression induced by emodin. Transfecting p53 siRNA also attenuated apoptosis induced by emodin, Bax expression and mitochondrial translocation being reduced compared to treatment with emodin alone. Taken together, these results indicate that ROS is a trigger of emodin-induced apoptosis in HCT116 cells, and p53 expression increases under oxidative stress, leading to Bax-mediated mitochondrial apoptosis.

#Emodin #Human colon cancer HCT116 cells #ROS #p53 #Mitochondrial apoptosis

참고문헌 (0)

참고문헌 신청

참고문헌이 DBpia에서 서비스 중이라면, [참고문헌 신청]을 통해 등록해보세요

이 논문의 저자 정보

Xie, Mei-Juan

소속기관 State Key Laboratory of Natural Medicines, School of Life Science and Technology, China Pharmaceutic