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: Metastatic breast tumors undergo epithelial-to-mesenchymal transition ( EMT ) , which renders them resistant to therapies targeted to the primary cancers . The mechanistic link between mtDNA ( mitochondrial DNA ) reduction , often seen in breast cancer patients , and EMT is unknown . We demonstrate that reducing mtDNA content in human mammary epithelial cells ( hMECs ) activates Calcineurin ( Cn)-dependent mitochondrial retrograde signaling pathway , which induces EMT-like reprogramming to fibroblastic morphology , loss of cell polarity , contact inhibition and acquired migratory and invasive phenotype . Notably , mtDNA reduction generates breast cancer stem cells . In addition to retrograde signaling markers , there is an induction of mesenchymal genes but loss of epithelial markers in these cells . The changes are reversed by either restoring the mtDNA content or knockdown of CnAÎ± mRNA , indicating the causal role of retrograde signaling in EMT . Our results point to a new therapeutic strategy for metastatic breast cancers targeted to the mitochondrial retrograde signaling pathway for abrogating EMT and attenuating cancer stem cells , which evade conventional therapies . We report a novel regulatory mechanism by which low mtDNA content generates EMT and cancer stem cells in hMECs.Oncogene advance online publication , 4 November 2013 ; doi:10.1038/onc.2013.467 .
    OUTPUT:

agent
activating invasion and metastasis;evading growth suppressors
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: Metastatic breast tumors undergo epithelial-to-mesenchymal transition ( EMT ) , which renders them resistant to therapies targeted to the primary cancers . The mechanistic link between mtDNA ( mitochondrial DNA ) reduction , often seen in breast cancer patients , and EMT is unknown . We demonstrate that reducing mtDNA content in human mammary epithelial cells ( hMECs ) activates Calcineurin ( Cn)-dependent mitochondrial retrograde signaling pathway , which induces EMT-like reprogramming to fibroblastic morphology , loss of cell polarity , contact inhibition and acquired migratory and invasive phenotype . Notably , mtDNA reduction generates breast cancer stem cells . In addition to retrograde signaling markers , there is an induction of mesenchymal genes but loss of epithelial markers in these cells . The changes are reversed by either restoring the mtDNA content or knockdown of CnAÎ± mRNA , indicating the causal role of retrograde signaling in EMT . Our results point to a new therapeutic strategy for metastatic breast cancers targeted to the mitochondrial retrograde signaling pathway for abrogating EMT and attenuating cancer stem cells , which evade conventional therapies . We report a novel regulatory mechanism by which low mtDNA content generates EMT and cancer stem cells in hMECs.Oncogene advance online publication , 4 November 2013 ; doi:10.1038/onc.2013.467 .
    OUTPUT:
