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: Glycolysis is the initial step of glucose catabolism and is up-regulated in cancer cells ( the Warburg Effect ) . Such shifts toward a glycolytic phenotype have not been explored widely in other biological systems , and the molecular mechanisms underlying the shifts remain unknown . With proteomics , we observed increased glycolysis in disused human diaphragm muscle . In disused muscle , lung cancer , and H(2)O(2)-treated myotubes , we show up-regulation of the rate-limiting glycolytic enzyme muscle-type phosphofructokinase ( PFKm , &gt;2 fold , P&lt;0.05 ) and accumulation of lactate ( &gt;150% , P&lt;0.05 ) . Using microRNA profiling , we identify miR-320a as a regulator of PFKm expression . Reduced miR-320a levels ( to ∼50% of control , P&lt;0.05 ) are associated with the increased PFKm in each of these diverse systems . Manipulation of miR-320a levels both in vitro and in vivo alters PFKm and lactate levels in the expected directions . Further , miR-320a appears to regulate oxidative stress-induced PFKm expression , and reduced miR-320a allows greater induction of glycolysis in response to H(2)O(2) treatment . We show that this microRNA-mediated regulation occurs through PFKm's 3 ' untranslated region and that Ets proteins are involved in the regulation of PFKm via miR-320a . These findings suggest that oxidative stress-responsive microRNA-320a may regulate glycolysis broadly within nature .
    OUTPUT:

agent
cellular energetics;tumor promoting inflammation
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: Glycolysis is the initial step of glucose catabolism and is up-regulated in cancer cells ( the Warburg Effect ) . Such shifts toward a glycolytic phenotype have not been explored widely in other biological systems , and the molecular mechanisms underlying the shifts remain unknown . With proteomics , we observed increased glycolysis in disused human diaphragm muscle . In disused muscle , lung cancer , and H(2)O(2)-treated myotubes , we show up-regulation of the rate-limiting glycolytic enzyme muscle-type phosphofructokinase ( PFKm , &gt;2 fold , P&lt;0.05 ) and accumulation of lactate ( &gt;150% , P&lt;0.05 ) . Using microRNA profiling , we identify miR-320a as a regulator of PFKm expression . Reduced miR-320a levels ( to ∼50% of control , P&lt;0.05 ) are associated with the increased PFKm in each of these diverse systems . Manipulation of miR-320a levels both in vitro and in vivo alters PFKm and lactate levels in the expected directions . Further , miR-320a appears to regulate oxidative stress-induced PFKm expression , and reduced miR-320a allows greater induction of glycolysis in response to H(2)O(2) treatment . We show that this microRNA-mediated regulation occurs through PFKm's 3 ' untranslated region and that Ets proteins are involved in the regulation of PFKm via miR-320a . These findings suggest that oxidative stress-responsive microRNA-320a may regulate glycolysis broadly within nature .
    OUTPUT:
