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 preferentially metabolize glucose through aerobic glycolysis . This phenomenon , known as the Warburg effect , is an anomalous characteristic of glucose metabolism in cancer cells . Chronic inflammation is a key promoting factor of tumourigenesis . It remains , however , largely unexplored whether and how pro-tumourigenic inflammation regulates glucose metabolism in cancer cells . Here , we show that pro-inflammatory cytokines promote glycolysis in breast cancer cells , and that the inflammation-induced miR-155 functions as an important mediator in this process . We further show that miR-155 acts to upregulate hexokinase 2 ( hk2 ) , through two distinct mechanisms . First , miR-155 promotes hk2 transcription by activation of signal transducer and activator of transcription 3 ( STAT3 ) , a transcriptional activator for hk2 . Second , via targeting C/EBPβ ( a transcriptional activator for mir-143 ) , miR-155 represses mir-143 , a negative regulator of hk2 , thus resulting in upregulation of hk2 expression at the post-transcriptional level . The miR-155-mediated hk2 upregulation also appears to operate in other types of cancer cells examined . We suggest that the miR-155/miR-143/HK2 axis may represent a common mechanism linking inflammation to the altered metabolism in cancer cells .
    OUTPUT:

agent
cellular energetics;tumor promoting inflammation
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 preferentially metabolize glucose through aerobic glycolysis . This phenomenon , known as the Warburg effect , is an anomalous characteristic of glucose metabolism in cancer cells . Chronic inflammation is a key promoting factor of tumourigenesis . It remains , however , largely unexplored whether and how pro-tumourigenic inflammation regulates glucose metabolism in cancer cells . Here , we show that pro-inflammatory cytokines promote glycolysis in breast cancer cells , and that the inflammation-induced miR-155 functions as an important mediator in this process . We further show that miR-155 acts to upregulate hexokinase 2 ( hk2 ) , through two distinct mechanisms . First , miR-155 promotes hk2 transcription by activation of signal transducer and activator of transcription 3 ( STAT3 ) , a transcriptional activator for hk2 . Second , via targeting C/EBPβ ( a transcriptional activator for mir-143 ) , miR-155 represses mir-143 , a negative regulator of hk2 , thus resulting in upregulation of hk2 expression at the post-transcriptional level . The miR-155-mediated hk2 upregulation also appears to operate in other types of cancer cells examined . We suggest that the miR-155/miR-143/HK2 axis may represent a common mechanism linking inflammation to the altered metabolism in cancer cells .
    OUTPUT:
