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 have elevated aerobic glycolysis that is termed the Warburg effect . But several tumor cells , including leukemic cells , also increase glutamine metabolism , which is initiated by glutaminase ( GLS ) . The microRNA ( miRNA ) miR-23 targets GLS mRNA and inhibits expression of GLS protein . Here we show that in human leukemic Jurkat cells the NF-ÎºB p65 subunit binds to miR-23a promoter and inhibits miR-23a expression . Histone deacetylase ( HDAC ) inhibitors release p65-induced inhibition . Jurkat cells growing in glutamine decrease proliferation due to cell accumulation in G0/G1 phase . Nevertheless , cells get used to this new source of energy by increasing GLS expression , which correlates with an increase in p65 expression and its translocation to the nucleus , leading to a higher basal NF-ÎºB activity . Jurkat cells overexpressing p65 show increase basal GLS expression and proliferate faster than control cells in glutamine medium . Overexpressing miR-23a in leukemic cells impaired glutamine use and induces mitochondrial dysfunction leading to cell death . Therefore , p65 activation decreases miR-23a expression , which facilitates glutamine consumption allowing leukemic cells to use this alternative source of carbon and favoring their adaptation to the metabolic environment .
    OUTPUT:

agent
sustaining proliferative signaling;cellular energetics
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: Cancer cells have elevated aerobic glycolysis that is termed the Warburg effect . But several tumor cells , including leukemic cells , also increase glutamine metabolism , which is initiated by glutaminase ( GLS ) . The microRNA ( miRNA ) miR-23 targets GLS mRNA and inhibits expression of GLS protein . Here we show that in human leukemic Jurkat cells the NF-ÎºB p65 subunit binds to miR-23a promoter and inhibits miR-23a expression . Histone deacetylase ( HDAC ) inhibitors release p65-induced inhibition . Jurkat cells growing in glutamine decrease proliferation due to cell accumulation in G0/G1 phase . Nevertheless , cells get used to this new source of energy by increasing GLS expression , which correlates with an increase in p65 expression and its translocation to the nucleus , leading to a higher basal NF-ÎºB activity . Jurkat cells overexpressing p65 show increase basal GLS expression and proliferate faster than control cells in glutamine medium . Overexpressing miR-23a in leukemic cells impaired glutamine use and induces mitochondrial dysfunction leading to cell death . Therefore , p65 activation decreases miR-23a expression , which facilitates glutamine consumption allowing leukemic cells to use this alternative source of carbon and favoring their adaptation to the metabolic environment .
    OUTPUT:
