A benzylideneacetophenone derivative induces apoptosis of radiation-resistant human breast cancer cells via oxidative stress
- 주제(키워드) Apoptosis , Benzylideneacetophenone derivative , Radiation resistance , Reactive oxygen species
- 후원정보 Ministry of Education, Science and Technology
- 등재 SCIE, SCOPUS, KCI등재
- 발행기관 Korean Society of Applied Pharmacology
- 발행년도 2017
- URI http://www.dcollection.net/handler/ewha/000000155850
- 본문언어 영어
- Published As http://dx.doi.org/10.4062/biomolther.2017.010
- 저작권 이화여자대학교 논문은 저작권에 의해 보호받습니다.
초록/요약
Benzylideneacetophenone derivative (1E)-1-(4-hydroxy-3-methoxyphenyl) hept-1-en-3-one (JC3) elicited cytotoxic effects on MDA-MB 231 human breast cancer cells-radiation resistant cells (MDA-MB 231-RR), in a dose-dependent manner, with an IC50 value of 6 μM JC3. JC3-mediated apoptosis was confirmed by increase in sub-G1 cell population. JC3 disrupted the mitochondrial membrane potential, and reduced expression of anti-apoptotic B cell lymphoma-2 protein, whereas it increased expression of pro-apoptotic Bcl-2-associated X protein, leading to the cleavage of caspase-9, caspase-3 and poly (ADP-ribose) polymerase. In addition, JC3 activated mitogen-activated protein kinases, and specific inhibitors of these kinases abrogated the JC3-induced increase in apoptotic bodies. JC3 increased the level of intracellular reactive oxygen species and enhanced oxidative macromolecular damage via lipid peroxidation, protein carbonylation, and DNA strand breakage. Considering these findings, JC3 is an effective therapy against radiation-resistant human breast cancer cells. © 2017 The Korean Society of Applied Pharmacology.
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