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KMID : 0358420110540040175
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Korean Journal of Obstetrics and Gynecology
2011 Volume.54 No. 4 p.175 ~ p.183
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THE EFFECT OF CISPLATIN ON ENDOPLASMIC RETICULUM STRESS OF HUMAN CERVICAL CANCER CELLS
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Kim Hun-Young
Kim Byoung-Ryun
Kim Kang-Deuk
Kim Hyung-Jin
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Abstract
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Objective : Cis-diamminedichloroplatinum (cisplatin) is a widely used chemotherapeutic agent. A number of evidences in cytotoxic mechanism of cisplatin, including perturbation of redox status, increase in lipid peroxydation, formation of DNA adduct, have been suggested. The author hypothesized that cisplatin would mediate apoptosis via endoplasmic reticulum (ER) stress in human cervical cancer cell.
Methods: Human cervical cancer cell line (Hela cells) were treated with cisplatin and then ER stress-related response were performed using western blot, Flow cytometry and fl uorescence analysis.
Results: After addition of cisplatin to Hela cells, the author observed an expression of ER stress response genes through a gradual increase of nitric oxide and cytosolic Ca2+ concentration. Cisplatin-induced apoptosis can be inhibited by the inducible nitric oxide synthase inhibitor, 1400 W, and intracellular Ca2+ chelator, 1, 2-bis-(o-aminophenoxy)ethane-N,N,N’,N’-tetraacetic acid tetra-(acetoxymethyl) ester (BAPTA-AM). These inhibitors also reduced mitochondrial apoptotic signals, such as mitochondrion membrane potential disruption, cytochrome c release and eventually reduced the death of Hela cells.
Conclusion: Taken together, ER would seem to contribute to cisplatin-induced apoptosis via both the early release of Ca2+ and the late amplifi cation of mitochondria-mediated apoptotic signals.
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KEYWORD
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Cisplatin, Endoplasmic reticulum stress, Cervical cancer cells
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