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논문 기본 정보

자료유형
학술저널
저자정보
He, Lin (Department of Pathology, Institute of Neuroscience, Chongqing Key Laboratory of Neurobiology, Chongqing Medical University) Bi, Juan-Juan (Department of Pathology, Institute of Neuroscience, Chongqing Key Laboratory of Neurobiology, Chongqing Medical University) Guo, Qian (Department of Pathology, Institute of Neuroscience, Chongqing Key Laboratory of Neurobiology, Chongqing Medical University) Yu, Yin (Department of Pathology, Institute of Neuroscience, Chongqing Key Laboratory of Neurobiology, Chongqing Medical University) Ye, Xiu-Feng (Department of Pathology, Institute of Neuroscience, Chongqing Key Laboratory of Neurobiology, Chongqing Medical University)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제13권 제4호
발행연도
2012.1
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1,505 - 1,510 (6page)

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To aim of this was to observe emodin-mediated cytotoxicity and its influence on Rad51 and ERCC1 expressionin non-small cell lung cancer (NSCLC). NSCLC cells were cultured in vitro with emodin at various concentrations (0, 25, 50, 75 and $100\;{\mu}mol/L$) for 48h and the proliferation inhibition rate was determined by the MTT method. Then, NSCLC were treated with emodin (SK-MES-1 $40\;{\mu}mol/L$, A549 $70\;{\mu}mol/L$) or $20\;{\mu}mol/L$ U0126 (an ERK inhibitor) for 48 h, or with various concentrations of emodin for 48 h and the protein and mRNA expressions of ERCC1 and Rad51 were determined by RT-PCR and Western blot assay, respectively. Emodin exerted a suppressive effect on the proliferation of NSCLC in a concentration dependent manner. Protein and mRNA expression of ERCC1 and Rad51 was also significantly decreased with the dose. Vacuolar degeneration was observed in A549 and SK-MES-1 cell lines after emodin treatment by transmission electron microscopy. Emodin may thus inhibited cell proliferation in NSCLC cells by downregulation ERCC1 and Rad51.

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