human
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: Vascular integrity is fundamental to the formation of mature blood vessels and depends on a functional , quiescent endothelial monolayer . However , how endothelial cells enter and maintain quiescence in the presence of angiogenic factors is still poorly understood . Here we identify the fibroblast growth factor ( FGF ) antagonist Sprouty2 ( Spry2 ) as a key player in mediating endothelial quiescence and barrier integrity in mouse aortic endothelial cells ( MAECs ) : Spry2 knockout MAECs show spindle-like shapes and are incapable of forming a functional , impermeable endothelial monolayer in the presence of FGF2 . Whereas dense wild type cells exhibit contact inhibition and stop to proliferate , Spry2 knockout MAECs remain responsive to FGF2 and continue to proliferate even at high cell densities . Importantly , the anti-proliferative effect of Spry2 is absent in sparsely plated cells . This cell density-dependent Spry2 function correlates with highly increased Spry2 expression in confluent wild type MAECs . Spry2 protein expression is barely detectable in single cells but steadily increases in cells growing to high cell densities , with hypoxia being one contributing factor . At confluence , Spry2 expression correlates with intact cell-cell contacts , whereas disruption of cell-cell contacts by EGTA , TNFÎ± and thrombin decreases Spry2 protein expression . In confluent cells , high Spry2 levels correlate with decreased extracellular signal-regulated kinase 1/2 ( Erk1/2 ) phosphorylation . In contrast , dense Spry2 knockout MAECs exhibit enhanced signaling by Erk1/2 . Moreover , inhibiting Erk1/2 activity in Spry2 knockout cells restores wild type cobblestone monolayer morphology . This study thus reveals a novel Spry2 function , which mediates endothelial contact inhibition and barrier integrity .
    OUTPUT:

agent
evading growth suppressors
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
    ###
    INPUT: Vascular integrity is fundamental to the formation of mature blood vessels and depends on a functional , quiescent endothelial monolayer . However , how endothelial cells enter and maintain quiescence in the presence of angiogenic factors is still poorly understood . Here we identify the fibroblast growth factor ( FGF ) antagonist Sprouty2 ( Spry2 ) as a key player in mediating endothelial quiescence and barrier integrity in mouse aortic endothelial cells ( MAECs ) : Spry2 knockout MAECs show spindle-like shapes and are incapable of forming a functional , impermeable endothelial monolayer in the presence of FGF2 . Whereas dense wild type cells exhibit contact inhibition and stop to proliferate , Spry2 knockout MAECs remain responsive to FGF2 and continue to proliferate even at high cell densities . Importantly , the anti-proliferative effect of Spry2 is absent in sparsely plated cells . This cell density-dependent Spry2 function correlates with highly increased Spry2 expression in confluent wild type MAECs . Spry2 protein expression is barely detectable in single cells but steadily increases in cells growing to high cell densities , with hypoxia being one contributing factor . At confluence , Spry2 expression correlates with intact cell-cell contacts , whereas disruption of cell-cell contacts by EGTA , TNFÎ± and thrombin decreases Spry2 protein expression . In confluent cells , high Spry2 levels correlate with decreased extracellular signal-regulated kinase 1/2 ( Erk1/2 ) phosphorylation . In contrast , dense Spry2 knockout MAECs exhibit enhanced signaling by Erk1/2 . Moreover , inhibiting Erk1/2 activity in Spry2 knockout cells restores wild type cobblestone monolayer morphology . This study thus reveals a novel Spry2 function , which mediates endothelial contact inhibition and barrier integrity .
    OUTPUT:
