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: OBJECTIVE Chronic generation of inflammatory cytokines and reactive oxygen species are implicated in atherosclerosis , aging , cancers , and other chronic diseases . We hypothesized that zinc induces A20 in premonocytic , endothelial , and cancer cells , and A20 binds to tumor necrosis factor ( TNF)-receptor associated factor , and inhibits IÎº kinase-Î± ( IKK-Î±)/nuclear factor-ÎºB ( NF-ÎºB ) , resulting in downregulation of TNF-Î± and interleukin-1Î² ( IL-1Î² ) . METHODS To test this hypothesis , we used HL-60 , human umbilical vein endothelial cells , and SW480 cell lines under zinc-deficient and zinc-sufficient conditions in this study . We measured oxidative stress markers , inflammatory cytokines , A20 protein and mRNA , A20-FRAF-1 complex , and IKK-Î±/NF-ÎºB signaling in stimulated zinc-deficient and zinc sufficient cells . We also conducted antisense A20 and siRNA studies to investigate the regulatory role of zinc in TNF-Î± and IL-1Î² via A20 . RESULTS We found that zinc increased A20 and A20-tumor necrosis factor-receptor associated factor-1 complex , decreased the IKK-Î±/NF-ÎºB signaling pathway , oxidative stress markers , and inflammatory cytokines in these cells compared with zinc-deficient cells . We confirmed that zinc-induced A20 contributes to downregulation of TNF-Î± and IL-1Î² by antisense and short interfering RNA A20 studies . CONCLUSION Our studies suggest that zinc suppresses generation of NF-ÎºB-regulated inflammatory cytokines by induction of A20 .
    OUTPUT:

agent
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: OBJECTIVE Chronic generation of inflammatory cytokines and reactive oxygen species are implicated in atherosclerosis , aging , cancers , and other chronic diseases . We hypothesized that zinc induces A20 in premonocytic , endothelial , and cancer cells , and A20 binds to tumor necrosis factor ( TNF)-receptor associated factor , and inhibits IÎº kinase-Î± ( IKK-Î±)/nuclear factor-ÎºB ( NF-ÎºB ) , resulting in downregulation of TNF-Î± and interleukin-1Î² ( IL-1Î² ) . METHODS To test this hypothesis , we used HL-60 , human umbilical vein endothelial cells , and SW480 cell lines under zinc-deficient and zinc-sufficient conditions in this study . We measured oxidative stress markers , inflammatory cytokines , A20 protein and mRNA , A20-FRAF-1 complex , and IKK-Î±/NF-ÎºB signaling in stimulated zinc-deficient and zinc sufficient cells . We also conducted antisense A20 and siRNA studies to investigate the regulatory role of zinc in TNF-Î± and IL-1Î² via A20 . RESULTS We found that zinc increased A20 and A20-tumor necrosis factor-receptor associated factor-1 complex , decreased the IKK-Î±/NF-ÎºB signaling pathway , oxidative stress markers , and inflammatory cytokines in these cells compared with zinc-deficient cells . We confirmed that zinc-induced A20 contributes to downregulation of TNF-Î± and IL-1Î² by antisense and short interfering RNA A20 studies . CONCLUSION Our studies suggest that zinc suppresses generation of NF-ÎºB-regulated inflammatory cytokines by induction of A20 .
    OUTPUT:
