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: Aberrant glucose metabolism characterized by high levels of glycolysis , even in the presence of oxygen , is an important hallmark of cancer . This metabolic reprogramming referred to as the Warburg effect is essential to the survival of tumor cells and provides them with substrates required for biomass generation . Molecular mechanisms responsible for this shift in glucose metabolism remain elusive . As described herein , we found that aberrant expression of the proinflammatory protein transglutaminase 2 ( TG2 ) is an important regulator of the Warburg effect in mammary epithelial cells . Mechanistically , TG2 regulated metabolic reprogramming by constitutively activating nuclear factor ( NF)-κB , which binds to the hypoxia-inducible factor ( HIF)-1α promoter and induces its expression even under normoxic conditions . TG2/NF-κB-induced increase in HIF-1α expression was associated with increased glucose uptake , increased lactate production and decreased oxygen consumption by mitochondria . Experimental suppression of TG2 attenuated HIF-1α expression and reversed downstream events in mammary epithelial cells . Moreover , downregulation of p65/RelA or HIF-1α expression in these cells restored normal glucose uptake , lactate production , mitochondrial respiration and glycolytic protein expression . Our results suggest that aberrant expression of TG2 is a master regulator of metabolic reprogramming and facilitates metabolic alterations in epithelial cells even under normoxic conditions . A TG2-induced shift in glucose metabolism helps breast cancer cells to survive under stressful conditions and promotes their metastatic competence .
    OUTPUT:

agent
cellular energetics;tumor promoting inflammation;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: Aberrant glucose metabolism characterized by high levels of glycolysis , even in the presence of oxygen , is an important hallmark of cancer . This metabolic reprogramming referred to as the Warburg effect is essential to the survival of tumor cells and provides them with substrates required for biomass generation . Molecular mechanisms responsible for this shift in glucose metabolism remain elusive . As described herein , we found that aberrant expression of the proinflammatory protein transglutaminase 2 ( TG2 ) is an important regulator of the Warburg effect in mammary epithelial cells . Mechanistically , TG2 regulated metabolic reprogramming by constitutively activating nuclear factor ( NF)-κB , which binds to the hypoxia-inducible factor ( HIF)-1α promoter and induces its expression even under normoxic conditions . TG2/NF-κB-induced increase in HIF-1α expression was associated with increased glucose uptake , increased lactate production and decreased oxygen consumption by mitochondria . Experimental suppression of TG2 attenuated HIF-1α expression and reversed downstream events in mammary epithelial cells . Moreover , downregulation of p65/RelA or HIF-1α expression in these cells restored normal glucose uptake , lactate production , mitochondrial respiration and glycolytic protein expression . Our results suggest that aberrant expression of TG2 is a master regulator of metabolic reprogramming and facilitates metabolic alterations in epithelial cells even under normoxic conditions . A TG2-induced shift in glucose metabolism helps breast cancer cells to survive under stressful conditions and promotes their metastatic competence .
    OUTPUT:
