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: Compound C , a well-known inhibitor of the intracellular energy sensor AMP-activated protein kinase ( AMPK ) , has been reported to cause apoptotic cell death in myeloma , breast cancer cells and glioma cells . In this study , we have demonstrated that compound C not only induced autophagy in all tested skin cancer cell lines but also caused more apoptosis in p53 wildtype skin cancer cells than in p53-mutant skin cancer cells . Compound C can induce upregulation , phosphorylation and nuclear translocalization of the p53 protein and upregulate expression of p53 target genes in wildtype p53-expressing skin basal cell carcinoma ( BCC ) cells . The changes of p53 status were dependent on DNA damage which was caused by compound C induced reactive oxygen species ( ROS ) generation and associated with activated ataxia-telangiectasia mutated ( ATM ) protein . Using the wildtype p53-expressing BCC cells versus stable p53-knockdown BCC sublines , we present evidence that p53-knockdown cancer cells were much less sensitive to compound C treatment with significant G2/M cell cycle arrest and attenuated the compound C-induced apoptosis but not autophagy . The compound C induced G2/M arrest in p53-knockdown BCC cells was associated with the sustained inactive Tyr15 phosphor-Cdc2 expression . Overall , our results established that compound C-induced apoptosis in skin cancer cells was dependent on the cell's p53 status .
    OUTPUT:

agent
resisting cell death;genomic instability and mutation;tumor promoting inflammation;evading growth suppressors;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: Compound C , a well-known inhibitor of the intracellular energy sensor AMP-activated protein kinase ( AMPK ) , has been reported to cause apoptotic cell death in myeloma , breast cancer cells and glioma cells . In this study , we have demonstrated that compound C not only induced autophagy in all tested skin cancer cell lines but also caused more apoptosis in p53 wildtype skin cancer cells than in p53-mutant skin cancer cells . Compound C can induce upregulation , phosphorylation and nuclear translocalization of the p53 protein and upregulate expression of p53 target genes in wildtype p53-expressing skin basal cell carcinoma ( BCC ) cells . The changes of p53 status were dependent on DNA damage which was caused by compound C induced reactive oxygen species ( ROS ) generation and associated with activated ataxia-telangiectasia mutated ( ATM ) protein . Using the wildtype p53-expressing BCC cells versus stable p53-knockdown BCC sublines , we present evidence that p53-knockdown cancer cells were much less sensitive to compound C treatment with significant G2/M cell cycle arrest and attenuated the compound C-induced apoptosis but not autophagy . The compound C induced G2/M arrest in p53-knockdown BCC cells was associated with the sustained inactive Tyr15 phosphor-Cdc2 expression . Overall , our results established that compound C-induced apoptosis in skin cancer cells was dependent on the cell's p53 status .
    OUTPUT:
