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: A common metabolic change in cancer is the acquisition of glycolytic phenotypes . Increased expression of glycolytic enzymes is considered as one contributing factor . The role of mitochondrial defects in acquisition of glycolytic phenotypes has been postulated but remains controversial . Here we show that functional defects in mitochondrial respiration could be induced by oncogenic H-Ras(Q61L) transformation , even though the mitochondrial contents or mass was not reduced in the transformed cells . First , mitochondrial respiration , as measured by mitochondrial oxygen consumption , was suppressed in NIH-3T3 cells transformed with H-Ras(Q61L) . Second , oligomycin or rotenone did not reduce the cellular ATP levels in the H-Ras(Q61L) transformed cells , suggesting a diminished role of mitochondrial respiration in the cellular energy metabolism . Third , inhibition of glycolysis with iodoacetic acid reduced ATP levels at a much faster rate in H-Ras(Q61L) transformed cells than in the vector control cells . The reduction of cellular ATP levels was reversed by exogenously added pyruvate in the vector control cells but not in H-Ras(Q61L) transformed cells . Finally when compared to the HRas(Q61L) transformed cells , the vector control cells had increased resistance toward glucose deprivation . The increased resistance was dependent on mitochondrial oxidative phosphorylation since rotenone or oligomycin abolished the increased survival of the vector control cells under glucose deprivation . The results also suggest an inability of the H-Ras(Q61L) transformed cells to reactivate mitochondrial respiration under glucose deprivation . Taken together , the data suggest that mitochondrial respiration can be impaired during transformation of NIH-3T3 cells by oncogeneic H-Ras(Q61L) .
    OUTPUT:

agent
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: A common metabolic change in cancer is the acquisition of glycolytic phenotypes . Increased expression of glycolytic enzymes is considered as one contributing factor . The role of mitochondrial defects in acquisition of glycolytic phenotypes has been postulated but remains controversial . Here we show that functional defects in mitochondrial respiration could be induced by oncogenic H-Ras(Q61L) transformation , even though the mitochondrial contents or mass was not reduced in the transformed cells . First , mitochondrial respiration , as measured by mitochondrial oxygen consumption , was suppressed in NIH-3T3 cells transformed with H-Ras(Q61L) . Second , oligomycin or rotenone did not reduce the cellular ATP levels in the H-Ras(Q61L) transformed cells , suggesting a diminished role of mitochondrial respiration in the cellular energy metabolism . Third , inhibition of glycolysis with iodoacetic acid reduced ATP levels at a much faster rate in H-Ras(Q61L) transformed cells than in the vector control cells . The reduction of cellular ATP levels was reversed by exogenously added pyruvate in the vector control cells but not in H-Ras(Q61L) transformed cells . Finally when compared to the HRas(Q61L) transformed cells , the vector control cells had increased resistance toward glucose deprivation . The increased resistance was dependent on mitochondrial oxidative phosphorylation since rotenone or oligomycin abolished the increased survival of the vector control cells under glucose deprivation . The results also suggest an inability of the H-Ras(Q61L) transformed cells to reactivate mitochondrial respiration under glucose deprivation . Taken together , the data suggest that mitochondrial respiration can be impaired during transformation of NIH-3T3 cells by oncogeneic H-Ras(Q61L) .
    OUTPUT:
