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: INTRODUCTION IÎºB Kinase Îµ ( IKKÎµ ) is a member of the IKK family which plays an important role in the activation of nuclear factor-ÎºB ( NF-ÎºB ) . Overexpressed in over 30% of breast cancers , IKKÎµ has been recently identified as a potential breast cancer oncogene . The purpose of this study is to examine the therapeutic potential of IKKÎµ siRNA on human breast cancer cells . METHODS Eight siRNAs targeting different regions of the IKKÎµ mRNA were designed , and the silencing effect was screened by quantitative real time RT-PCR . The biological effects of synthetic siRNAs on human breast cancer cells were investigated by examining the cell proliferation , migration , invasion , focus formation , anchorage-independent growth(via soft agar assay ) , cell cycle arrest , apoptosis ( via annexing binding ) , NF-ÎºB basal level , and NF-ÎºB related gene expressions upon the IKKÎµ silencing . RESULTS Silencing of IKKÎµ in human breast cancer cells resulted in decrease of focus formation potential and clonogenicity as well as in vitro cell migration/invasion capabilities . Moreover , knockdown of IKKÎµ suppressed cell proliferation . Cell cycle assay showed that the anti-proliferation effect of IKKÎµ siRNA was mediated by arresting cells in G(0)/G(1) phase , which was caused by down-regulation of cyclin D(1) . Furthermore , we demonstrated that silencing of IKKÎµ inhibited the NF-ÎºB basal activity as well as the Bcl-2 expression . Significant apoptosis was not observed in breast cancer cells upon the silencing of IKKÎµ . The present study provided the first evidence that silencing IKKÎµ using synthetic siRNA could inhibit the invasiveness properties and proliferation of breast cancer cells . CONCLUSIONS Our results suggested that silencing IKKÎµ using synthetic siRNA may offer a novel therapeutic strategy for breast cancer .
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agent
activating invasion and metastasis;evading growth suppressors;sustaining proliferative signaling;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.
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    INPUT: INTRODUCTION IÎºB Kinase Îµ ( IKKÎµ ) is a member of the IKK family which plays an important role in the activation of nuclear factor-ÎºB ( NF-ÎºB ) . Overexpressed in over 30% of breast cancers , IKKÎµ has been recently identified as a potential breast cancer oncogene . The purpose of this study is to examine the therapeutic potential of IKKÎµ siRNA on human breast cancer cells . METHODS Eight siRNAs targeting different regions of the IKKÎµ mRNA were designed , and the silencing effect was screened by quantitative real time RT-PCR . The biological effects of synthetic siRNAs on human breast cancer cells were investigated by examining the cell proliferation , migration , invasion , focus formation , anchorage-independent growth(via soft agar assay ) , cell cycle arrest , apoptosis ( via annexing binding ) , NF-ÎºB basal level , and NF-ÎºB related gene expressions upon the IKKÎµ silencing . RESULTS Silencing of IKKÎµ in human breast cancer cells resulted in decrease of focus formation potential and clonogenicity as well as in vitro cell migration/invasion capabilities . Moreover , knockdown of IKKÎµ suppressed cell proliferation . Cell cycle assay showed that the anti-proliferation effect of IKKÎµ siRNA was mediated by arresting cells in G(0)/G(1) phase , which was caused by down-regulation of cyclin D(1) . Furthermore , we demonstrated that silencing of IKKÎµ inhibited the NF-ÎºB basal activity as well as the Bcl-2 expression . Significant apoptosis was not observed in breast cancer cells upon the silencing of IKKÎµ . The present study provided the first evidence that silencing IKKÎµ using synthetic siRNA could inhibit the invasiveness properties and proliferation of breast cancer cells . CONCLUSIONS Our results suggested that silencing IKKÎµ using synthetic siRNA may offer a novel therapeutic strategy for breast cancer .
    OUTPUT:
