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: Silver nanoparticles ( Ag-np ) have been used in medicine and commercially due to their anti-microbial properties . Therapeutic potentials of these nanoparticles are being explored extensively despite the lack of information on their mechanism of action at molecular and cellular level . Here , we have investigated the DNA damage response and repair following Ag-np treatment in mammalian cells . Studies have shown that Ag-np exerts genotoxicity through double-strand breaks ( DSBs ) . DNA-PKcs , the catalytic subunit of DNA dependent protein kinase , is an important caretaker of the genome which is known to be the main player mediating Non-homologous End-Joining ( NHEJ ) repair pathway . We hypothesize that DNA-PKcs is responsible for the repair of Ag-np induced DNA damage . In vitro studies have been carried out to investigate both cytotoxicity and genotoxicity induced by Ag-np in normal human cells , DNA-PKcs proficient , and deficient mammalian cells . Chemical inhibition of DNA-PKcs activity with NU7026 , an ATP-competitive inhibitor of DNA-PKcs , has been performed to further validate the role of DNA-PKcs in this model . Our results suggest that Ag-np induced more prominent dose-dependent decrease in cell viability in DNA-PKcs deficient or inhibited cells . The deficiency or inhibition of DNA-PKcs renders the cells with higher susceptibility to DNA damage and genome instability which in turn contributed to greater cell cycle arrest/cell death . These findings support the fact that DNA-PKcs is involved in the repair of Ag-np induced genotoxicity and NHEJ repair pathway and DNA-PKcs particularly is activated to safeguard the genome upon Ag-np exposure .
    OUTPUT:

agent
genomic instability and mutation;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: Silver nanoparticles ( Ag-np ) have been used in medicine and commercially due to their anti-microbial properties . Therapeutic potentials of these nanoparticles are being explored extensively despite the lack of information on their mechanism of action at molecular and cellular level . Here , we have investigated the DNA damage response and repair following Ag-np treatment in mammalian cells . Studies have shown that Ag-np exerts genotoxicity through double-strand breaks ( DSBs ) . DNA-PKcs , the catalytic subunit of DNA dependent protein kinase , is an important caretaker of the genome which is known to be the main player mediating Non-homologous End-Joining ( NHEJ ) repair pathway . We hypothesize that DNA-PKcs is responsible for the repair of Ag-np induced DNA damage . In vitro studies have been carried out to investigate both cytotoxicity and genotoxicity induced by Ag-np in normal human cells , DNA-PKcs proficient , and deficient mammalian cells . Chemical inhibition of DNA-PKcs activity with NU7026 , an ATP-competitive inhibitor of DNA-PKcs , has been performed to further validate the role of DNA-PKcs in this model . Our results suggest that Ag-np induced more prominent dose-dependent decrease in cell viability in DNA-PKcs deficient or inhibited cells . The deficiency or inhibition of DNA-PKcs renders the cells with higher susceptibility to DNA damage and genome instability which in turn contributed to greater cell cycle arrest/cell death . These findings support the fact that DNA-PKcs is involved in the repair of Ag-np induced genotoxicity and NHEJ repair pathway and DNA-PKcs particularly is activated to safeguard the genome upon Ag-np exposure .
    OUTPUT:
