Yu, H.-C.H.-C.YuCHEN-SI LINTai, W.-T.W.-T.TaiLiu, C.-Y.C.-Y.LiuShiau, C.-W.C.-W.ShiauKuen-Feng Chen2018-09-102018-09-102013http://www.scopus.com/inward/record.url?eid=2-s2.0-84880070521&partnerID=MN8TOARShttp://scholars.lib.ntu.edu.tw/handle/123456789/377266Background: 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.[SDGs]SDG3Autophagy; 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 Assaysjournal article10.1074/jbc.M112.446385