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: The innate immune response involves a variety of inflammatory reactions that can result in inflammatory disease and cancer if they are not resolved and instead are allowed to persist . The effective activation and resolution of innate immune responses relies on the production and posttranscriptional regulation of mRNAs encoding inflammatory effector proteins . The RNA-binding protein HuR binds to and regulates such mRNAs , but its exact role in inflammation remains unclear . Here we show that HuR maintains inflammatory homeostasis by controlling macrophage plasticity and migration . Mice lacking HuR in myeloid-lineage cells , which include many of the cells of the innate immune system , displayed enhanced sensitivity to endotoxemia , rapid progression of chemical-induced colitis , and severe susceptibility to colitis-associated cancer . The myeloid cell-specific HuR-deficient mice had an exacerbated inflammatory cytokine profile and showed enhanced CCR2-mediated macrophage chemotaxis . At the molecular level , activated macrophages from these mice showed enhancements in the use of inflammatory mRNAs ( including Tnf , Tgfb , Il10 , Ccr2 , and Ccl2 ) due to a lack of inhibitory effects on their inducible translation and/or stability . Conversely , myeloid overexpression of HuR induced posttranscriptional silencing , reduced inflammatory profiles , and protected mice from colitis and cancer . Our results highlight the role of HuR as a homeostatic coordinator of mRNAs that encode molecules that guide innate inflammatory effects and demonstrate the potential of harnessing the effects of HuR for clinical benefit against pathologic inflammation and cancer .
    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: The innate immune response involves a variety of inflammatory reactions that can result in inflammatory disease and cancer if they are not resolved and instead are allowed to persist . The effective activation and resolution of innate immune responses relies on the production and posttranscriptional regulation of mRNAs encoding inflammatory effector proteins . The RNA-binding protein HuR binds to and regulates such mRNAs , but its exact role in inflammation remains unclear . Here we show that HuR maintains inflammatory homeostasis by controlling macrophage plasticity and migration . Mice lacking HuR in myeloid-lineage cells , which include many of the cells of the innate immune system , displayed enhanced sensitivity to endotoxemia , rapid progression of chemical-induced colitis , and severe susceptibility to colitis-associated cancer . The myeloid cell-specific HuR-deficient mice had an exacerbated inflammatory cytokine profile and showed enhanced CCR2-mediated macrophage chemotaxis . At the molecular level , activated macrophages from these mice showed enhancements in the use of inflammatory mRNAs ( including Tnf , Tgfb , Il10 , Ccr2 , and Ccl2 ) due to a lack of inhibitory effects on their inducible translation and/or stability . Conversely , myeloid overexpression of HuR induced posttranscriptional silencing , reduced inflammatory profiles , and protected mice from colitis and cancer . Our results highlight the role of HuR as a homeostatic coordinator of mRNAs that encode molecules that guide innate inflammatory effects and demonstrate the potential of harnessing the effects of HuR for clinical benefit against pathologic inflammation and cancer .
    OUTPUT:
