DOI QR코드

DOI QR Code

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

  • 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)
  • 발행 : 2014.07.15

초록

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.

키워드

참고문헌

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피인용 문헌

  1. Emodin: A Review of its Pharmacology, Toxicity and Pharmacokinetics vol.30, pp.8, 2016, https://doi.org/10.1002/ptr.5631
  2. Emodin induces hepatocellular carcinoma cell apoptosis through MAPK and PI3K/AKT signaling pathways in vitro and in vivo vol.36, pp.2, 2016, https://doi.org/10.3892/or.2016.4861
  3. Inhibitory effect of emodin on fatty acid synthase, colon cancer proliferation and apoptosis vol.15, pp.4, 2017, https://doi.org/10.3892/mmr.2017.6254
  4. Development of Certain Protein Kinase Inhibitors with the Components from Traditional Chinese Medicine vol.7, pp.1663-9812, 2017, https://doi.org/10.3389/fphar.2016.00523
  5. Chrysophanol induces cell death and inhibits invasiveness via mitochondrial calcium overload in ovarian cancer cells vol.119, pp.12, 2018, https://doi.org/10.1002/jcb.27363
  6. Drug Delivery System for Emodin Based on Mesoporous Silica SBA-15 vol.8, pp.5, 2018, https://doi.org/10.3390/nano8050322