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: Oxaliplatin is included in a number of effective combination regimens used as first and subsequent lines of therapy for metastatic colorectal cancer . Accumulating evidence indicates that autophagy plays a significant role in response to cancer therapy . However , the role of autophagy in oxaliplatin-induced cell death remains to be clarified . In this study , we showed that oxaliplatin induced cell death and autophagy in Caco-2 colorectal cancer cells . The suppression of autophagy using either pharmacologic inhibitors ( 3-methyladenine , bafilomycin A1 ) or RNA interference in essential autophagy genes ( ATG5 or Beclin1 ) enhanced the cell death and reactive oxygen species ( ROS ) production induced by oxaliplatin in Caco-2 cells . Blocking oxaliplatin-induced ROS production by using ROS scavengers ( NAC or Tiron ) decreased autophagy . Furthermore , numerous dilated endoplasmic reticula ( ER ) were present in oxaliplatin-treated Caco-2 cells , and blocking ER stress by RNA interference against candidate of metastasis-1 ( P8 ) and C/EBP-homologous protein ( CHOP ) decreased autophagy and ROS production . Taken together , these data indicate that oxaliplatin activates autophagy as a cytoprotective response via ER stress and ROS in human colorectal cancer cells .
    OUTPUT:

agent
resisting cell death;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.
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    INPUT: Oxaliplatin is included in a number of effective combination regimens used as first and subsequent lines of therapy for metastatic colorectal cancer . Accumulating evidence indicates that autophagy plays a significant role in response to cancer therapy . However , the role of autophagy in oxaliplatin-induced cell death remains to be clarified . In this study , we showed that oxaliplatin induced cell death and autophagy in Caco-2 colorectal cancer cells . The suppression of autophagy using either pharmacologic inhibitors ( 3-methyladenine , bafilomycin A1 ) or RNA interference in essential autophagy genes ( ATG5 or Beclin1 ) enhanced the cell death and reactive oxygen species ( ROS ) production induced by oxaliplatin in Caco-2 cells . Blocking oxaliplatin-induced ROS production by using ROS scavengers ( NAC or Tiron ) decreased autophagy . Furthermore , numerous dilated endoplasmic reticula ( ER ) were present in oxaliplatin-treated Caco-2 cells , and blocking ER stress by RNA interference against candidate of metastasis-1 ( P8 ) and C/EBP-homologous protein ( CHOP ) decreased autophagy and ROS production . Taken together , these data indicate that oxaliplatin activates autophagy as a cytoprotective response via ER stress and ROS in human colorectal cancer cells .
    OUTPUT:
