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: The vacuolar H+-ATPase ( V-ATPase ) , a multisubunit proton pump , has come into focus as an attractive target in cancer invasion . However little is known about the role of V-ATPase in cell death and especially the underlying mechanisms remain mostly unknown . We used the myxobacterial macrolide archazolid B , a potent inhibitor of the V-ATPase , as an experimental drug as well as a chemical tool to decipher V-ATPase related cell death signaling . We found that archazolid induced apoptosis in highly invasive tumor cells at nanomolar concentrations which was executed by the mitochondrial pathway . Prior to apoptosis induction archazolid lead to the activation of a cellular stress response including activation of the hypoxia-inducible factor-1 alpha ( HIF1alpha ) and autophagy . Autophagy was induced at low concentrations of archazolid that do not alter pH in lysosomes and was shown by degradation of p62 or fusion of autophagosomes with lysosomes . HIF1alpha was induced due to energy stress shown by a decline of the ATP level and followed by a shut down of energy consuming processes . As silencing HIF1alpha increases apoptosis , the cellular stress response was suggested to be a survival mechanism . We conclude that archazolid leads to energy stress which activates adaptive mechanisms like autophagy mediated by HIF1alpha and finally leads to apoptosis . We propose V-ATPase as a promising drugable target in cancer therapy caught up at the interplay of apoptosis , autophagy and cellular/metabolic stress .
    OUTPUT:

agent
resisting cell death
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: The vacuolar H+-ATPase ( V-ATPase ) , a multisubunit proton pump , has come into focus as an attractive target in cancer invasion . However little is known about the role of V-ATPase in cell death and especially the underlying mechanisms remain mostly unknown . We used the myxobacterial macrolide archazolid B , a potent inhibitor of the V-ATPase , as an experimental drug as well as a chemical tool to decipher V-ATPase related cell death signaling . We found that archazolid induced apoptosis in highly invasive tumor cells at nanomolar concentrations which was executed by the mitochondrial pathway . Prior to apoptosis induction archazolid lead to the activation of a cellular stress response including activation of the hypoxia-inducible factor-1 alpha ( HIF1alpha ) and autophagy . Autophagy was induced at low concentrations of archazolid that do not alter pH in lysosomes and was shown by degradation of p62 or fusion of autophagosomes with lysosomes . HIF1alpha was induced due to energy stress shown by a decline of the ATP level and followed by a shut down of energy consuming processes . As silencing HIF1alpha increases apoptosis , the cellular stress response was suggested to be a survival mechanism . We conclude that archazolid leads to energy stress which activates adaptive mechanisms like autophagy mediated by HIF1alpha and finally leads to apoptosis . We propose V-ATPase as a promising drugable target in cancer therapy caught up at the interplay of apoptosis , autophagy and cellular/metabolic stress .
    OUTPUT:
