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: Vasohibin-1 ( VASH1 ) is isolated as an endothelial cell ( EC)-produced angiogenesis inhibitor . We questioned whether VASH1 plays any role besides angiogenesis inhibition , knocked-down or overexpressed VASH1 in ECs , and examined the changes of EC property . Knock-down of VASH1 induced premature senescence of ECs , and those ECs were easily killed by cellular stresses . In contrast , overexpression of VASH1 made ECs resistant to premature senescence and cell death caused by cellular stresses . The synthesis of VASH1 was regulated by HuR-mediated post-transcriptional regulation . We sought to define the underlying mechanism . VASH1 increased the expression of ( superoxide dismutase 2 ) SOD2 , an enzyme known to quench reactive oxygen species ( ROS ) . Simultaneously , VASH1 augmented the synthesis of sirtuin 1 ( SIRT1 ) , an anti-aging protein , which improved stress tolerance . Paraquat generates ROS and causes organ damage when administered in vivo . More VASH1 ( +/- ) mice died due to acute lung injury caused by paraquat . Intratracheal administration of an adenovirus vector encoding human VASH1 augmented SOD2 and SIRT1 expression in the lungs and prevented acute lung injury caused by paraquat . Thus , VASH1 is a critical factor that improves the stress tolerance of ECs via the induction of SOD2 and SIRT1 .
    OUTPUT:

agent
tumor promoting inflammation
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: Vasohibin-1 ( VASH1 ) is isolated as an endothelial cell ( EC)-produced angiogenesis inhibitor . We questioned whether VASH1 plays any role besides angiogenesis inhibition , knocked-down or overexpressed VASH1 in ECs , and examined the changes of EC property . Knock-down of VASH1 induced premature senescence of ECs , and those ECs were easily killed by cellular stresses . In contrast , overexpression of VASH1 made ECs resistant to premature senescence and cell death caused by cellular stresses . The synthesis of VASH1 was regulated by HuR-mediated post-transcriptional regulation . We sought to define the underlying mechanism . VASH1 increased the expression of ( superoxide dismutase 2 ) SOD2 , an enzyme known to quench reactive oxygen species ( ROS ) . Simultaneously , VASH1 augmented the synthesis of sirtuin 1 ( SIRT1 ) , an anti-aging protein , which improved stress tolerance . Paraquat generates ROS and causes organ damage when administered in vivo . More VASH1 ( +/- ) mice died due to acute lung injury caused by paraquat . Intratracheal administration of an adenovirus vector encoding human VASH1 augmented SOD2 and SIRT1 expression in the lungs and prevented acute lung injury caused by paraquat . Thus , VASH1 is a critical factor that improves the stress tolerance of ECs via the induction of SOD2 and SIRT1 .
    OUTPUT:
