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 constantly adapt to oxidative phosphorylation ( OXPHOS ) suppression resulting from hypoxia or mitochondria defects . Under the OXPHOS suppression , AMP-activated protein kinase ( AMPK ) regulates global metabolism adjustments , but its activation has been found to be transient . Whether cells can maintain cellular ATP homeostasis and survive beyond the transient AMPK activation is not known . Here , we study the bioenergetic adaptation to the OXPHOS inhibitor oligomycin in a group of cancer cells . We found that oligomycin at 100 ng/ml completely inhibits OXPHOS activity in 1 h and induces various levels of glycolysis gains by 6 h , from which we calculate the bioenergetic organizations of cancer cells . In glycolysis-dominant cells , oligomycin does not induce much energy stress as measured by glycolysis acceleration , ATP imbalance , AMPK activation , AMPK substrate acetyl-CoA carboxylase phosphorylation at Ser(79) , and cell growth inhibition . In OXPHOS-dependent LKB1 wild type cells , oligomycin induces 5-8% ATP drops and transient AMPK activation during the initial 1-2 h . After AMPK activation is completed , oligomycin-induced increase of acetyl-CoA carboxylase phosphorylation at Ser(79) is still detected , and cellular ATP is back at preoligomycin treatment levels by sustained elevation of glycolysis . Cell growth , however , is inhibited without an increase in cell death and alteration in cell cycle distribution . In OXPHOS-dependent LKB1-null cells , no AMPK activation by oligomycin is detected , yet cells still show a similar adaptation . We also demonstrate that the adaptation to oligomycin does not invoke activation of hypoxia-induced factor . Our data suggest that cancer cells may grow and survive persistent OXPHOS suppression through an as yet unidentified regulatory mechanism .
    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: Cancer cells constantly adapt to oxidative phosphorylation ( OXPHOS ) suppression resulting from hypoxia or mitochondria defects . Under the OXPHOS suppression , AMP-activated protein kinase ( AMPK ) regulates global metabolism adjustments , but its activation has been found to be transient . Whether cells can maintain cellular ATP homeostasis and survive beyond the transient AMPK activation is not known . Here , we study the bioenergetic adaptation to the OXPHOS inhibitor oligomycin in a group of cancer cells . We found that oligomycin at 100 ng/ml completely inhibits OXPHOS activity in 1 h and induces various levels of glycolysis gains by 6 h , from which we calculate the bioenergetic organizations of cancer cells . In glycolysis-dominant cells , oligomycin does not induce much energy stress as measured by glycolysis acceleration , ATP imbalance , AMPK activation , AMPK substrate acetyl-CoA carboxylase phosphorylation at Ser(79) , and cell growth inhibition . In OXPHOS-dependent LKB1 wild type cells , oligomycin induces 5-8% ATP drops and transient AMPK activation during the initial 1-2 h . After AMPK activation is completed , oligomycin-induced increase of acetyl-CoA carboxylase phosphorylation at Ser(79) is still detected , and cellular ATP is back at preoligomycin treatment levels by sustained elevation of glycolysis . Cell growth , however , is inhibited without an increase in cell death and alteration in cell cycle distribution . In OXPHOS-dependent LKB1-null cells , no AMPK activation by oligomycin is detected , yet cells still show a similar adaptation . We also demonstrate that the adaptation to oligomycin does not invoke activation of hypoxia-induced factor . Our data suggest that cancer cells may grow and survive persistent OXPHOS suppression through an as yet unidentified regulatory mechanism .
    OUTPUT:
