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: Nucling is a stress-inducible protein associated with apoptosomes . The cytochrome c-triggered formation of apoptosomes represents a key-initiating event in apoptosis . We have recently reported that Nucling regulates the apoptotic pathway by controlling the activation of NF-kappaB as well . Here we show that hepatocellular carcinoma ( HCC ) arising spontaneously against a background of hepatitis occurred more frequently in Nucling-knockout ( KO ) mice than wild-type ( WT ) mice . Biochemical serum testing revealed potential liver dysfunction with hypercholesterolemia in Nucling-KO males . In the background of Nucling-KO mice , we observed the up-regulation of TNFalpha , spontaneous NF-kappaB-activation and the induction of galectin-3 expression in liver . In addition , we observed a decrease in the number of Kupffer cells ( KCs ) in the KO mice . KCs are important for the hepatic immune system , acting as phagocytes or antigen-presenting cells ( APCs ) . We found that KCs in Nucling-KO mice were apoptotic possibly through the up-regulation of TNFalpha . These observations indicate that Nucling is important for the regulation of NF-kappaB signals in liver . We propose that Nucling deficiency could be a powerful tool to reveal the NF-kappaB-related molecular networks leading to hepatitis and HCC development .
    OUTPUT:

agent
avoiding immune destruction;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: Nucling is a stress-inducible protein associated with apoptosomes . The cytochrome c-triggered formation of apoptosomes represents a key-initiating event in apoptosis . We have recently reported that Nucling regulates the apoptotic pathway by controlling the activation of NF-kappaB as well . Here we show that hepatocellular carcinoma ( HCC ) arising spontaneously against a background of hepatitis occurred more frequently in Nucling-knockout ( KO ) mice than wild-type ( WT ) mice . Biochemical serum testing revealed potential liver dysfunction with hypercholesterolemia in Nucling-KO males . In the background of Nucling-KO mice , we observed the up-regulation of TNFalpha , spontaneous NF-kappaB-activation and the induction of galectin-3 expression in liver . In addition , we observed a decrease in the number of Kupffer cells ( KCs ) in the KO mice . KCs are important for the hepatic immune system , acting as phagocytes or antigen-presenting cells ( APCs ) . We found that KCs in Nucling-KO mice were apoptotic possibly through the up-regulation of TNFalpha . These observations indicate that Nucling is important for the regulation of NF-kappaB signals in liver . We propose that Nucling deficiency could be a powerful tool to reveal the NF-kappaB-related molecular networks leading to hepatitis and HCC development .
    OUTPUT:
