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: Ceramide induces cell cycle arrest and apoptotic cell death associated with increased levels of p27(kip1) . The aim of this study was to examine the effects of ceramide on p27(kip1) protein levels as a measure of cell cycle arrest and apoptosis . Results showed that ceramide increased p27(kip1) protein levels through activation of protein phosphatase 2A ( PP2A ) in PC-3 prostate cancer cells . Treatment of cells with the PP2A inhibitor okadaic acid or with PP2A-CÎ± siRNA inhibited ceramide-induced enhanced p27(kip1) protein expression and Akt dephosphorylation , and prevented Skp2 downregulation . Overexpression of constitutively active Akt attenuated ceramide-induced Skp2 downregulation and p27(kip1) upregulation . In addition , ceramide stimulated binding of the PP2A catalytic subunit PP2A-CÎ±Î² to Akt as assessed by immunoprecipitation experiments , indicating that PP2A is involved in the induction of p27(kip1) via inhibition of Akt pathway . Finally , whether PP2A can regulate p27(kip1) expression independently of Akt pathway was determined . Knockdown of PP2A-CÎ± with siRNA reduced p27(kip1) levels in the presence of Akt inhibitor . These data reveal that PP2A is a regulator of ceramide-induced p27(kip1) expression via Akt-dependent and Akt-independent pathways .
    OUTPUT:

agent
evading growth suppressors;sustaining proliferative signaling
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: Ceramide induces cell cycle arrest and apoptotic cell death associated with increased levels of p27(kip1) . The aim of this study was to examine the effects of ceramide on p27(kip1) protein levels as a measure of cell cycle arrest and apoptosis . Results showed that ceramide increased p27(kip1) protein levels through activation of protein phosphatase 2A ( PP2A ) in PC-3 prostate cancer cells . Treatment of cells with the PP2A inhibitor okadaic acid or with PP2A-CÎ± siRNA inhibited ceramide-induced enhanced p27(kip1) protein expression and Akt dephosphorylation , and prevented Skp2 downregulation . Overexpression of constitutively active Akt attenuated ceramide-induced Skp2 downregulation and p27(kip1) upregulation . In addition , ceramide stimulated binding of the PP2A catalytic subunit PP2A-CÎ±Î² to Akt as assessed by immunoprecipitation experiments , indicating that PP2A is involved in the induction of p27(kip1) via inhibition of Akt pathway . Finally , whether PP2A can regulate p27(kip1) expression independently of Akt pathway was determined . Knockdown of PP2A-CÎ± with siRNA reduced p27(kip1) levels in the presence of Akt inhibitor . These data reveal that PP2A is a regulator of ceramide-induced p27(kip1) expression via Akt-dependent and Akt-independent pathways .
    OUTPUT:
