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: Cancer cells exhibit altered glucose metabolism characterized by a preference for aerobic glycolysis or the Warburg effect , and the cells resist matrix detachment-induced apoptosis , which is called anoikis , a barrier to metastasis . It remains largely unclear whether tumor metabolism influences anoikis and metastasis . Here we show that when detached from the matrix , untransformed mammary epithelial cells undergo metabolic reprogramming by markedly upregulating pyruvate dehydrogenase ( PDH ) kinase 4 ( PDK4 ) through estrogen-related receptor gamma ( ERRγ ) , thereby inhibiting PDH and attenuating the flux of glycolytic carbon into mitochondrial oxidation . To decipher the significance of this metabolic response , we found that depletion of PDK4 or activation of PDH increased mitochondrial respiration and oxidative stress in suspended cells , resulting in heightened anoikis . Conversely , overexpression of PDKs prolonged survival of cells in suspension . Therefore , decreased glucose oxidation following cell detachment confers anoikis resistance . Unlike untransformed cells , most cancer cells demonstrate reduced glucose oxidation even under attached conditions , and thus they inherently possess a survival advantage when suspended . Normalization of glucose metabolism by stimulating PDH in cancer cells restores their susceptibility to anoikis and impairs their metastatic potential . These results suggest that the Warburg effect , more specifically , diminished glucose oxidation , promotes anoikis resistance and metastasis and that PDKs are potential targets for antimetastasis therapy .
    OUTPUT:

agent
cellular energetics;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.
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    INPUT: Cancer cells exhibit altered glucose metabolism characterized by a preference for aerobic glycolysis or the Warburg effect , and the cells resist matrix detachment-induced apoptosis , which is called anoikis , a barrier to metastasis . It remains largely unclear whether tumor metabolism influences anoikis and metastasis . Here we show that when detached from the matrix , untransformed mammary epithelial cells undergo metabolic reprogramming by markedly upregulating pyruvate dehydrogenase ( PDH ) kinase 4 ( PDK4 ) through estrogen-related receptor gamma ( ERRγ ) , thereby inhibiting PDH and attenuating the flux of glycolytic carbon into mitochondrial oxidation . To decipher the significance of this metabolic response , we found that depletion of PDK4 or activation of PDH increased mitochondrial respiration and oxidative stress in suspended cells , resulting in heightened anoikis . Conversely , overexpression of PDKs prolonged survival of cells in suspension . Therefore , decreased glucose oxidation following cell detachment confers anoikis resistance . Unlike untransformed cells , most cancer cells demonstrate reduced glucose oxidation even under attached conditions , and thus they inherently possess a survival advantage when suspended . Normalization of glucose metabolism by stimulating PDH in cancer cells restores their susceptibility to anoikis and impairs their metastatic potential . These results suggest that the Warburg effect , more specifically , diminished glucose oxidation , promotes anoikis resistance and metastasis and that PDKs are potential targets for antimetastasis therapy .
    OUTPUT:
