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: BACKGROUND Non-alcoholic fatty liver disease ( NAFLD ) is associated with obesity , insulin resistance and hepatic steatosis . Non-alcoholic steatohepatitis ( NASH ) is a serious consequence of NAFLD where chronic tissue damage and inflammation result in fibrosis which may progress to cirrhosis . Transforming growth factor beta1 ( TGFbeta1 ) , proinflammatory cytokines and oxidative stress are thought to play crucial roles in the pathogenesis of these conditions . The contributions of individual liver cell types to fibrogenesis remain controversial and the influence of selenium status has not been investigated . METHODS In this study we have used a cell culture model of fat-loading using oleate-treated human hepatoblastoma ( C3A ) cells to investigate how fat-loading and selenium status might influence the production of collagen in response to TGFbeta1 . The secretion of inflammatory cytokines was also investigated , together with the epithelial character of the treated cells . RESULTS We found that in response to treatment with TGFbeta1 , C3A cells produced mRNA encoding the pro-alphaI chain of procollagen I , secreted procollagen I peptide , up-regulated production of the proinflammatory cytokine interleukin-8 ( IL-8 ) and the mesenchymal marker vimentin , and down-regulated albumin production . Most of these responses were considerably enhanced when cells were fat-loaded with oleate and were attenuated by selenium addition at a dose that optimised the expression of thioredoxin reductase and glutathione peroxidase . CONCLUSIONS Our data establish that both fat-loading and suboptimal selenium status enhance collagen and IL-8 production by C3A hepatocytes in response to TGFbeta1 , possibly as part of an epithelial to mesenchymal transition . GENERAL SIGNIFICANCE These findings suggest that the hepatocyte may be an important contributor to the pathogenesis of fibrosis associated with NAFLD .
    OUTPUT:

agent
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.
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    INPUT: BACKGROUND Non-alcoholic fatty liver disease ( NAFLD ) is associated with obesity , insulin resistance and hepatic steatosis . Non-alcoholic steatohepatitis ( NASH ) is a serious consequence of NAFLD where chronic tissue damage and inflammation result in fibrosis which may progress to cirrhosis . Transforming growth factor beta1 ( TGFbeta1 ) , proinflammatory cytokines and oxidative stress are thought to play crucial roles in the pathogenesis of these conditions . The contributions of individual liver cell types to fibrogenesis remain controversial and the influence of selenium status has not been investigated . METHODS In this study we have used a cell culture model of fat-loading using oleate-treated human hepatoblastoma ( C3A ) cells to investigate how fat-loading and selenium status might influence the production of collagen in response to TGFbeta1 . The secretion of inflammatory cytokines was also investigated , together with the epithelial character of the treated cells . RESULTS We found that in response to treatment with TGFbeta1 , C3A cells produced mRNA encoding the pro-alphaI chain of procollagen I , secreted procollagen I peptide , up-regulated production of the proinflammatory cytokine interleukin-8 ( IL-8 ) and the mesenchymal marker vimentin , and down-regulated albumin production . Most of these responses were considerably enhanced when cells were fat-loaded with oleate and were attenuated by selenium addition at a dose that optimised the expression of thioredoxin reductase and glutathione peroxidase . CONCLUSIONS Our data establish that both fat-loading and suboptimal selenium status enhance collagen and IL-8 production by C3A hepatocytes in response to TGFbeta1 , possibly as part of an epithelial to mesenchymal transition . GENERAL SIGNIFICANCE These findings suggest that the hepatocyte may be an important contributor to the pathogenesis of fibrosis associated with NAFLD .
    OUTPUT:
