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10.5483/bmbrep.2016.49.9.069

http://scihub22266oqcxt.onion/10.5483/bmbrep.2016.49.9.069
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27439603!5227144!27439603
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suck abstract from ncbi


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pmid27439603      BMB+Rep 2016 ; 49 (9): 508-13
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  • Suppression of Akt-HIF-1alpha signaling axis by diacetyl atractylodiol inhibits hypoxia-induced angiogenesis #MMPMID27439603
  • Choi SW; Lee KS; Lee JH; Kang HJ; Lee MJ; Kim HY; Park KI; Kim SL; Shin HK; Seo WD
  • BMB Rep 2016[Sep]; 49 (9): 508-13 PMID27439603show ga
  • Hypoxia-inducible factor (HIF)-1alpha is a key regulator associated with tumorigenesis, angiogenesis, and metastasis. HIF-1alpha regulation under hypoxia has been highlighted as a promising therapeutic target in angiogenesis-related diseases. Here, we demonstrate that diacetyl atractylodiol (DAA) from Atractylodes japonica (A. japonica) is a potent HIF-1alpha inhibitor that inhibits the Akt signaling pathway. DAA dose-dependently inhibited hypoxia-induced HIF-1alpha and downregulated Akt signaling without affecting the stability of HIF-1alpha protein. Furthermore, DAA prevented hypoxia-mediated angiogenesis based on in vitro tube formation and in vivo chorioallantoic membrane (CAM) assays. Therefore, DAA might be useful for treatment of hypoxia-related tumorigenesis, including angiogenesis. [BMB Reports 2016; 49(9): 508-513].
  • |Atractylodes/chemistry/metabolism[MESH]
  • |Blotting, Western[MESH]
  • |Chorioallantoic Membrane/drug effects/physiology[MESH]
  • |Cobalt/toxicity[MESH]
  • |Down-Regulation/drug effects[MESH]
  • |Enediynes/*pharmacology[MESH]
  • |HeLa Cells[MESH]
  • |Human Umbilical Vein Endothelial Cells[MESH]
  • |Humans[MESH]
  • |Hypoxia-Inducible Factor 1, alpha Subunit/genetics/*metabolism[MESH]
  • |Neovascularization, Physiologic/*drug effects[MESH]
  • |Phosphorylation/drug effects[MESH]
  • |Proto-Oncogene Proteins c-akt/*metabolism[MESH]
  • |Real-Time Polymerase Chain Reaction[MESH]
  • |Signal Transduction/*drug effects[MESH]


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