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: Although interleukin-28A ( IL-28A ) is believed to have an antiviral effect , its role in tumor migration requires further examination . The present study was intended to verify the effect of IL-28A on the migration of UMUC-3 bladder cancer cells . IL-28A and its receptor IL-28AR1 mRNA were detected in UMUC-3 cells . Although exogenous IL-28A showed no effect on cell proliferation , a wound-healing migration assay showed that the migration of UMUC-3 cells was induced by IL-28A . Furthermore , treatment of the cells with IL-28A significantly promoted MMP-9 expression via binding activities of NF-ÎºB and AP-1 . IL-28A also induced the activation of p38MAPK and Jak2-Stat2 signaling . Using the p38MAPK inhibitor SB203580 and the dominant-negative plasmid DN-p38 , we found evidence that the inhibition of p38MAPK signaling suppressed the effects of IL-28A including wound-healing migration and MMP-9 expression by activation of NF-ÎºB and AP-1 binding in UMUC-3 cells . However , Jak-2 inhibition by AG490 did not affect IL-28A-induced migration of UMUC-3 cells . Collectively , we suggest for the first time that the p38MAPK pathway mediates IL-28A-induced cell migration through MMP-9 expression by activating NF-ÎºB and AP-1 binding motifs .
    OUTPUT:

agent
sustaining proliferative signaling;activating invasion and metastasis
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: Although interleukin-28A ( IL-28A ) is believed to have an antiviral effect , its role in tumor migration requires further examination . The present study was intended to verify the effect of IL-28A on the migration of UMUC-3 bladder cancer cells . IL-28A and its receptor IL-28AR1 mRNA were detected in UMUC-3 cells . Although exogenous IL-28A showed no effect on cell proliferation , a wound-healing migration assay showed that the migration of UMUC-3 cells was induced by IL-28A . Furthermore , treatment of the cells with IL-28A significantly promoted MMP-9 expression via binding activities of NF-ÎºB and AP-1 . IL-28A also induced the activation of p38MAPK and Jak2-Stat2 signaling . Using the p38MAPK inhibitor SB203580 and the dominant-negative plasmid DN-p38 , we found evidence that the inhibition of p38MAPK signaling suppressed the effects of IL-28A including wound-healing migration and MMP-9 expression by activation of NF-ÎºB and AP-1 binding in UMUC-3 cells . However , Jak-2 inhibition by AG490 did not affect IL-28A-induced migration of UMUC-3 cells . Collectively , we suggest for the first time that the p38MAPK pathway mediates IL-28A-induced cell migration through MMP-9 expression by activating NF-ÎºB and AP-1 binding motifs .
    OUTPUT:
