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A benzylideneacetophenone derivative induces apoptosis of radiation-resistant human breast cancer cells via oxidative stress

Title
A benzylideneacetophenone derivative induces apoptosis of radiation-resistant human breast cancer cells via oxidative stress
Authors
Hyun Y.J.Oh S.K.Jeong Y.J.Chae S.Hyun J.W.Park J.E.Piao M.J.Kang K.A.Shilnikova K.
Ewha Authors
오세관
SCOPUS Author ID
오세관scopus
Issue Date
2017
Journal Title
Biomolecules and Therapeutics
ISSN
1976-9148JCR Link
Citation
Biomolecules and Therapeutics vol. 25, no. 4, pp. 404 - 410
Keywords
ApoptosisBenzylideneacetophenone derivativeRadiation resistanceReactive oxygen species
Publisher
Korean Society of Applied Pharmacology
Indexed
SCIE; SCOPUS; KCI scopus
Document Type
Article
Abstract
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.
DOI
10.4062/biomolther.2017.010
Appears in Collections:
의과대학 > 의학과 > Journal papers
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