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논문 기본 정보

자료유형
학술저널
저자정보
Cho, Seung Hee (College of Pharmacy, Medical Research Center, Chungbuk National University) Park, Mi Hee (College of Pharmacy, Medical Research Center, Chungbuk National University) Lee, Hee Peom (College of Pharmacy, Medical Research Center, Chungbuk National University) Back, Myong Ki (College of Pharmacy, Medical Research Center, Chungbuk National University) Sung, Ha Chang (College of Pharmacy, Medical Research Center, Chungbuk National University) Chang, Hee Won (College of Pharmacy, Medical Research Center, Chungbuk National University) Kim, Joo Hwan (Osong Health Technology Administration Complex) Jeong, Heon-Sang (Agriculture, Life and Environments Sciences, Chungbuk National University) Han, Sang Bae (College of Pharmacy, Medical Research Center, Chungbuk National University) Hong, Jin Tae (College of Pharmacy, Medical Research Center, Chungbuk National University)
저널정보
대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제37권 제5호
발행연도
2014.1
수록면
652 - 661 (10page)

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Ovarian cancer is a cancerous growth arising from the ovary and with poor prognosis that usually have resistant to all currently available treatments. Whether (E)-2,4-bis(p-hydroxyphenyl)-2-butenal (butenal) synthesized by Maillard reaction from fructose-tyrosine, has potential therapeutic activity against human ovarian cancer was investigated using two ovarian cancer cell lines (PA-1, SK-OV-3). We found that butenal could inhibit NF-${\kappa}B$/STAT3 activity, thereby inducing apoptotic cell death of ovarian cancer cells. We treated with several concentration of butenal each cell line differently (PA-1; 5, 10 and $15{\mu}g/ml$, SK-OV-3; 10, 20 and $30{\mu}g/ml$). First, ovarian cancer cell lines exhibited constitutively active NF-${\kappa}B$, and treatment with butenal abolished this activation as indicated by DNA binding activity. Second, butenal suppressed activation of signal transducer and activator of transcription-3 as indicated by decreased phosphorylation and inhibition of Janus kinase-2 phosphorylation. Third, butenal induced expression of pro-apoptotic proteins such as proteolytic cleavage of PARP, Bax and activation of caspase-3, -8 and -9. Lastly, combination of butenal and TRAIL causes enhanced induction of apoptosis. Overall, our results indicate that butenal mediates its anti-proliferative and apoptotic effects through activation of multiple cell signaling pathways and enhances the TRAIL-induced apoptosis. These data suggested that butenal may be a potential anti-cancer agent in ovarian cancer.

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