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 upregulate glycolysis , increasing glucose uptake to meet energy needs . A small fraction of a cell's glucose enters the hexosamine biosynthetic pathway ( HBP ) , which regulates levels of O-linked beta-N-acetylglucosamine ( O-GlcNAc ) , a carbohydrate posttranslational modification of diverse nuclear and cytosolic proteins . We discovered that breast cancer cells upregulate the HBP , including increased O-GlcNAcation and elevated expression of O-GlcNAc transferase ( OGT ) , which is the enzyme catalyzing the addition of O-GlcNAc to proteins . Reduction of O-GlcNAcation through RNA interference of OGT in breast cancer cells leads to inhibition of tumor growth both in vitro and in vivo and is associated with decreased cell-cycle progression and increased expression of the cell-cycle inhibitor p27(Kip1) . Elevation of p27(Kip1) was associated with decreased expression and activity of the oncogenic transcription factor FoxM1 , a known regulator of p27(Kip1) stability through transcriptional control of Skp2 . Reducing O-GlcNAc levels in breast cancer cells decreased levels of FoxM1 protein and caused a decrease in multiple FoxM1-specific targets , including Skp2 . Moreover , reducing O-GlcNAcation decreased cancer cell invasion and was associated with the downregulation of matrix metalloproteinase-2 , a known FoxM1 target . Finally , pharmacological inhibition of OGT in breast cancer cells had similar anti-growth and anti-invasion effects . These findings identify O-GlcNAc as a novel mechanism through which alterations in glucose metabolism regulate cancer growth and invasion and suggest that OGT may represent novel therapeutic targets for breast cancer .
    OUTPUT:

agent
evading growth suppressors;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.
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    INPUT: Cancer cells upregulate glycolysis , increasing glucose uptake to meet energy needs . A small fraction of a cell's glucose enters the hexosamine biosynthetic pathway ( HBP ) , which regulates levels of O-linked beta-N-acetylglucosamine ( O-GlcNAc ) , a carbohydrate posttranslational modification of diverse nuclear and cytosolic proteins . We discovered that breast cancer cells upregulate the HBP , including increased O-GlcNAcation and elevated expression of O-GlcNAc transferase ( OGT ) , which is the enzyme catalyzing the addition of O-GlcNAc to proteins . Reduction of O-GlcNAcation through RNA interference of OGT in breast cancer cells leads to inhibition of tumor growth both in vitro and in vivo and is associated with decreased cell-cycle progression and increased expression of the cell-cycle inhibitor p27(Kip1) . Elevation of p27(Kip1) was associated with decreased expression and activity of the oncogenic transcription factor FoxM1 , a known regulator of p27(Kip1) stability through transcriptional control of Skp2 . Reducing O-GlcNAc levels in breast cancer cells decreased levels of FoxM1 protein and caused a decrease in multiple FoxM1-specific targets , including Skp2 . Moreover , reducing O-GlcNAcation decreased cancer cell invasion and was associated with the downregulation of matrix metalloproteinase-2 , a known FoxM1 target . Finally , pharmacological inhibition of OGT in breast cancer cells had similar anti-growth and anti-invasion effects . These findings identify O-GlcNAc as a novel mechanism through which alterations in glucose metabolism regulate cancer growth and invasion and suggest that OGT may represent novel therapeutic targets for breast cancer .
    OUTPUT:
