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: Perlecan Domain V ( DV ) promotes brain angiogenesis by inducing VEGF release from brain endothelial cells ( BECs ) following stroke . In this study , we define the specific mechanism of DV interaction with the Î±(5)Î²(1) integrin , identify the downstream signal transduction pathway , and further investigate the functional significance of resultant VEGF release . Interestingly , we found that the LG3 portion of DV , which has been suggested to possess most of DV's angio-modulatory activity outside of the brain , binds poorly to Î±(5)Î²(1) and induces less BEC proliferation compared to full length DV . Additionally , we implicate DV's DGR sequence as an important element for the interaction of DV with Î±(5)Î²(1) . Furthermore , we investigated the importance of AKT and ERK signaling in DV-induced VEGF expression and secretion . We show that DV increases the phosphorylation of ERK , which leads to subsequent activation and stabilization of eIF4E and HIF-1Î± . Inhibition of ERK activity by U0126 suppressed DV-induced expression and secretion of VEGR in BECs . While DV was capable of phosphorylating AKT we show that AKT phosphorylation does not play a role in DV's induction of VEGF expression or secretion using two separate inhibitors , LY294002 and Akt IV . Lastly , we demonstrate that VEGF activity is critical for DV increases in BEC proliferation , as well as angiogenesis in a BEC-neuronal co-culture system . Collectively , our findings expand our understanding of DV's mechanism of action on BECs , and further support its potential as a novel stroke therapy .
    OUTPUT:

agent
inducing angiogenesis;sustaining proliferative signaling
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: Perlecan Domain V ( DV ) promotes brain angiogenesis by inducing VEGF release from brain endothelial cells ( BECs ) following stroke . In this study , we define the specific mechanism of DV interaction with the Î±(5)Î²(1) integrin , identify the downstream signal transduction pathway , and further investigate the functional significance of resultant VEGF release . Interestingly , we found that the LG3 portion of DV , which has been suggested to possess most of DV's angio-modulatory activity outside of the brain , binds poorly to Î±(5)Î²(1) and induces less BEC proliferation compared to full length DV . Additionally , we implicate DV's DGR sequence as an important element for the interaction of DV with Î±(5)Î²(1) . Furthermore , we investigated the importance of AKT and ERK signaling in DV-induced VEGF expression and secretion . We show that DV increases the phosphorylation of ERK , which leads to subsequent activation and stabilization of eIF4E and HIF-1Î± . Inhibition of ERK activity by U0126 suppressed DV-induced expression and secretion of VEGR in BECs . While DV was capable of phosphorylating AKT we show that AKT phosphorylation does not play a role in DV's induction of VEGF expression or secretion using two separate inhibitors , LY294002 and Akt IV . Lastly , we demonstrate that VEGF activity is critical for DV increases in BEC proliferation , as well as angiogenesis in a BEC-neuronal co-culture system . Collectively , our findings expand our understanding of DV's mechanism of action on BECs , and further support its potential as a novel stroke therapy .
    OUTPUT:
