https://scholars.lib.ntu.edu.tw/handle/123456789/377266
標題: | Nilotinib induces autophagy in hepatocellular carcinoma through AMPK activation | 作者: | Yu, H.-C. CHEN-SI LIN Tai, W.-T. Liu, C.-Y. Shiau, C.-W. Kuen-Feng Chen |
公開日期: | 2013 | 卷: | 288 | 期: | 25 | 起(迄)頁: | 18249-18259 | 來源出版物: | Journal of Biological Chemistry | 摘要: | Background: Nilotinib, an approved drug for leukemia, has been investigated in HCC. Results: Nilotinib induced autophagy in HCC cell lines, including PLC5, Huh-7, and Hep3B. Conclusion: Nilotinib-induced AMPK activation and subsequent autophagy is a major mode of action of nilotinib in HCC. Significance: Elucidating the mechanisms by which nilotinib works on HCC is fundamental to develop the new treatment for HCC. ? 2013 by The American Society. |
URI: | http://www.scopus.com/inward/record.url?eid=2-s2.0-84880070521&partnerID=MN8TOARS http://scholars.lib.ntu.edu.tw/handle/123456789/377266 |
DOI: | 10.1074/jbc.M112.446385 | SDG/關鍵字: | Autophagy; Cell lines; Hepatocellular carcinoma; Mode of action; Nilotinib; Biochemistry; Biology; Cell culture; 3 methyladenine; acridine orange; adenylate kinase; caspase 3; caspase 8; caspase 9; hydroxychloroquine; microtubule associated protein; microtubule associated protein 1 light chain 3; nilotinib; phosphoprotein phosphatase 2A; sorafenib; unclassified drug; animal experiment; animal model; antineoplastic activity; apoptosis; article; autophagy; cancer cell culture; cancer growth; cancer inhibition; concentration response; controlled study; drug dose comparison; enzyme activation; enzyme activity; enzyme inactivation; enzyme phosphorylation; enzyme regulation; human; human cell; in vivo study; liver cell carcinoma; male; mouse; nonhuman; priority journal; protein expression; time; tumor xenograft; upregulation; Western blotting; AMP-activated Kinase (AMPK); Apoptosis; Autophagy; HCC; Nilotinib; Serine Threonine Protein Phosphatase; Tyrosine Protein Kinase (Tyrosine Kinase); Administration, Oral; AMP-Activated Protein Kinases; Animals; Autophagy; Blotting, Western; Carcinoma, Hepatocellular; Cell Line, Tumor; Cell Survival; Dose-Response Relationship, Drug; Enzyme Activation; Humans; Liver Neoplasms; Mice; Mice, Inbred BALB C; Mice, Nude; Phosphorylation; Protein Phosphatase 2; Pyrimidines; Time Factors; Xenograft Model Antitumor Assays |
顯示於: | 獸醫學系 |
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