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 Î²2-adrenergic receptor ( Î²2AR ) mediates the effects of chronic stress in several neoplasms , however , Î²2AR signaling is impaired by hypoxia in various tissues . While hypoxia is a common feature significant in the progression of solid tumors , little is known about the effect of hypoxia on Î²2AR signaling in the tumor microenvironment . Previously , it has been reported that the systemic administration of mesenchymal stem cells ( MSCs ) increased the engraftment and metastatic colonization of rat osteosarcoma ( OS ) cells . In the current study , the effect of MSCs on the hypoxia-induced desensitization of the Î²2AR in OS cells was investigated . Epinephrine , norepinephrine and isoproterenol increased the cellular proliferation of the rat OS cell line COS1NR and rat MSCs in a dose-dependent and Î²2AR antagonist-sensitive manner . While isoproterenol had significant proliferative effects on MSCs under normoxic and hypoxic conditions , COS1NR cells did not respond under hypoxic conditions . A sensitivity assay for the Î²2AR revealed that hypoxia impaired the sensitivity of COS1NR cells , whereas hypoxia did not affect MSCs . An immunoassay revealed no significant change in the expression of hypoxia-inducible factor-1Î± ( HIF1Î± ) in COS1NR cells , whilst an immunoassay demonstrated a 15% increase in MSCs following isoproterenol stimulation . In COS1NR cells co-cultured with MSCs under hypoxic conditions , isoproterenol caused a significant increase in proliferation and this effect was inhibited by an anti-interleukin ( IL)-6 antibody . A tumor formation assay in syngeneic rats revealed that the systemic administration of MSCs enhances the growth of OS and the effect of MSCs was inhibited by IL-6 neutralization . In conclusion , MSCs are resistant to the hypoxia-induced desensitization to Î²2AR . Hypoxia caused a siginificant desensitization of the Î²2AR in COS1NR cells alone , whereas MSCs may support tumor progression through cellular interactions .
    OUTPUT:

agent
sustaining proliferative signaling
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: The Î²2-adrenergic receptor ( Î²2AR ) mediates the effects of chronic stress in several neoplasms , however , Î²2AR signaling is impaired by hypoxia in various tissues . While hypoxia is a common feature significant in the progression of solid tumors , little is known about the effect of hypoxia on Î²2AR signaling in the tumor microenvironment . Previously , it has been reported that the systemic administration of mesenchymal stem cells ( MSCs ) increased the engraftment and metastatic colonization of rat osteosarcoma ( OS ) cells . In the current study , the effect of MSCs on the hypoxia-induced desensitization of the Î²2AR in OS cells was investigated . Epinephrine , norepinephrine and isoproterenol increased the cellular proliferation of the rat OS cell line COS1NR and rat MSCs in a dose-dependent and Î²2AR antagonist-sensitive manner . While isoproterenol had significant proliferative effects on MSCs under normoxic and hypoxic conditions , COS1NR cells did not respond under hypoxic conditions . A sensitivity assay for the Î²2AR revealed that hypoxia impaired the sensitivity of COS1NR cells , whereas hypoxia did not affect MSCs . An immunoassay revealed no significant change in the expression of hypoxia-inducible factor-1Î± ( HIF1Î± ) in COS1NR cells , whilst an immunoassay demonstrated a 15% increase in MSCs following isoproterenol stimulation . In COS1NR cells co-cultured with MSCs under hypoxic conditions , isoproterenol caused a significant increase in proliferation and this effect was inhibited by an anti-interleukin ( IL)-6 antibody . A tumor formation assay in syngeneic rats revealed that the systemic administration of MSCs enhances the growth of OS and the effect of MSCs was inhibited by IL-6 neutralization . In conclusion , MSCs are resistant to the hypoxia-induced desensitization to Î²2AR . Hypoxia caused a siginificant desensitization of the Î²2AR in COS1NR cells alone , whereas MSCs may support tumor progression through cellular interactions .
    OUTPUT:
