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.
    ###
    INPUT: BACKGROUND Autotaxin ( ATX ) is an extracellular lysophospholipase D that generates lysophosphatidic acid ( LPA ) from lysophosphatidylcholine ( LPC ) . Both ATX and LPA have been shown to be involved in many cancers . However , the functional role of ATX and the regulation of ATX expression in human hepatocellular carcinoma ( HCC ) remain elusive . RESULTS In this study , ATX expression was evaluated in tissues from 38 human HCC and 10 normal control subjects . ATX was detected mainly in tumor cells within tissue sections and its over-expression in HCC was specifically correlated with inflammation and liver cirrhosis . In addition , ATX expression was examined in normal human hepatocytes and liver cancer cell lines . Hepatoma Hep3B and Huh7 cells displayed stronger ATX expression than hepatoblastoma HepG2 cells and normal hepatocytes did . Proinflammtory cytokine tumor necrosis factor alpha ( TNF-alpha ) promoted ATX expression and secretion selectively in Hep3B and Huh7 cells , which led to a corresponding increase in lysophospholipase-D activity . Moreover , we explored the mechanism governing the expression of ATX in hepatoma cells and established a critical role of nuclear factor-kappa B ( NF-kappaB ) in basal and TNF-alpha induced ATX expression . Further study showed that secreted enzymatically active ATX stimulated Hep3B cell invasion . CONCLUSIONS This report highlights for the first time the clinical and biological evidence for the involvement of ATX in human HCC . Our observation that links the TNF-alpha/NF-kappaB axis and the ATX-LPA signaling pathway suggests that ATX is likely playing an important role in inflammation related liver tumorigenesis .
    OUTPUT:

agent
tumor promoting inflammation;activating invasion and metastasis
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: BACKGROUND Autotaxin ( ATX ) is an extracellular lysophospholipase D that generates lysophosphatidic acid ( LPA ) from lysophosphatidylcholine ( LPC ) . Both ATX and LPA have been shown to be involved in many cancers . However , the functional role of ATX and the regulation of ATX expression in human hepatocellular carcinoma ( HCC ) remain elusive . RESULTS In this study , ATX expression was evaluated in tissues from 38 human HCC and 10 normal control subjects . ATX was detected mainly in tumor cells within tissue sections and its over-expression in HCC was specifically correlated with inflammation and liver cirrhosis . In addition , ATX expression was examined in normal human hepatocytes and liver cancer cell lines . Hepatoma Hep3B and Huh7 cells displayed stronger ATX expression than hepatoblastoma HepG2 cells and normal hepatocytes did . Proinflammtory cytokine tumor necrosis factor alpha ( TNF-alpha ) promoted ATX expression and secretion selectively in Hep3B and Huh7 cells , which led to a corresponding increase in lysophospholipase-D activity . Moreover , we explored the mechanism governing the expression of ATX in hepatoma cells and established a critical role of nuclear factor-kappa B ( NF-kappaB ) in basal and TNF-alpha induced ATX expression . Further study showed that secreted enzymatically active ATX stimulated Hep3B cell invasion . CONCLUSIONS This report highlights for the first time the clinical and biological evidence for the involvement of ATX in human HCC . Our observation that links the TNF-alpha/NF-kappaB axis and the ATX-LPA signaling pathway suggests that ATX is likely playing an important role in inflammation related liver tumorigenesis .
    OUTPUT:
