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자료유형
학술저널
저자정보
Kim, Jung-Hee (Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University) Kim, Hee-Jong (Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University) Bak, Ye-Sol (Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University) Kang, Jeong-Woo (Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University) Lee, Dong-Hun (Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University) Kim, Man-Sub (Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University) Park, Yun-Sun (Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University) Kim, Eun-Jin (Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University) Jung, Kang-Yeoun (Department of Biochemical Engineering, College of Engineering, Gangneung-Wonju National University) Lim, Yoong-Ho (Department of Bioscience and Biotechnology, Bio/Molecular Informatics Center, Konkuk University) Hong, Jin-Tae (College of Pharma) Yoon, Do-Young
저널정보
한국응용생명화학회 Applied Biological Chemistry Applied Biological Chemistry 제55권 제1호
발행연도
2012.1
수록면
75 - 82 (8page)

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Anti-cancer effects of naringenin derivative diethyl (5,4'-dihydroxy flavanone-7-yl) phosphate were evaluated in human lung cancer cells. The effect of diethyl (5,4'-dihydroxy flavanone-7-yl) phosphate (dEdHF-7-p) on A549 cell viability was measured using MTS assay and cell counting. Morphological changes were detected using phase-contrast microscopy. Apoptosis was analyzed using Hoechst staining. The influence of dEdHF-7-p on cell cycle distribution was determined using propidium iodide (PI) staining, and protein expression was determined by Western blot analysis. A newly synthesized naringenin derivative dEdHF-7-p suppressed cell growth of A549 though mechanisms including inhibition of cell cycle and increased apoptosis. Apoptotic and cell cycle modulators were changed by dEdHF-7-p in A549 cells; cyclins, ppRB, and anti-apoptotic factor Bcl-2 were down-regulated, whereas apoptotic factor Bax and cyclin-dependent kinase inhibitors p21 and p53 were enhanced, thereby releasing cytochrome c into the cytosol of dEdHF-7-p-treated-A549 cells. dEdHF-7-p treatment processed caspases-3/-8/-9 and cleavage of poly ADP-ribose polymerase. The dEdHF-7-p treatment enhanced Fas expression and decreased expression of cell survival factors such as PI3K and p-Akt in a dose-dependent manner. Taken together, dEdHF-7-p induces apoptosis by inhibiting the PI3K/Akt survival signaling pathway and modulating mitochondria-emanated intrinsic and Fas extrinsic pathways in A549 cells.

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