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 is a sphingolipid metabolite that induces cancer cell death . When C6-ceramide is encapsulated in a nanoliposome bilayer formulation , cell death is selectively induced in tumor models . However , the mechanism underlying this selectivity is unknown . As most tumors exhibit a preferential switch to glycolysis , as described in the " Warburg effect " , we hypothesize that ceramide nanoliposomes selectively target this glycolytic pathway in cancer . We utilize chronic lymphocytic leukemia ( CLL ) as a cancer model , which has an increased dependency on glycolysis . In CLL cells , we demonstrate that C6-ceramide nanoliposomes , but not control nanoliposomes , induce caspase 3/7-independent necrotic cell death . Nanoliposomal ceramide inhibits both the RNA and protein expression of GAPDH , an enzyme in the glycolytic pathway , which is overexpressed in CLL . To confirm that ceramide targets GAPDH , we demonstrate that downregulation of GAPDH potentiates the decrease in ATP after ceramide treatment and exogenous pyruvate treatment as well as GAPDH overexpression partially rescues ceramide-induced necrosis . Finally , an in vivo murine model of CLL shows that nanoliposomal C6-ceramide treatment elicits tumor regression , concomitant with GAPDH downregulation . We conclude that selective inhibition of the glycolytic pathway in CLL cells with nanoliposomal C6-ceramide could potentially be an effective therapy for leukemia by targeting the Warburg effect .
    OUTPUT:

agent
resisting cell death;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: Ceramide is a sphingolipid metabolite that induces cancer cell death . When C6-ceramide is encapsulated in a nanoliposome bilayer formulation , cell death is selectively induced in tumor models . However , the mechanism underlying this selectivity is unknown . As most tumors exhibit a preferential switch to glycolysis , as described in the " Warburg effect " , we hypothesize that ceramide nanoliposomes selectively target this glycolytic pathway in cancer . We utilize chronic lymphocytic leukemia ( CLL ) as a cancer model , which has an increased dependency on glycolysis . In CLL cells , we demonstrate that C6-ceramide nanoliposomes , but not control nanoliposomes , induce caspase 3/7-independent necrotic cell death . Nanoliposomal ceramide inhibits both the RNA and protein expression of GAPDH , an enzyme in the glycolytic pathway , which is overexpressed in CLL . To confirm that ceramide targets GAPDH , we demonstrate that downregulation of GAPDH potentiates the decrease in ATP after ceramide treatment and exogenous pyruvate treatment as well as GAPDH overexpression partially rescues ceramide-induced necrosis . Finally , an in vivo murine model of CLL shows that nanoliposomal C6-ceramide treatment elicits tumor regression , concomitant with GAPDH downregulation . We conclude that selective inhibition of the glycolytic pathway in CLL cells with nanoliposomal C6-ceramide could potentially be an effective therapy for leukemia by targeting the Warburg effect .
    OUTPUT:
