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: CDA-2 ( cell differentiation agent 2 ) , a urinary preparation , has potent anti- proliferative and pro-apoptotic properties in cancer cells . However , the mechanisms of tumor inhibitory action of CDA-2 are far from clear , and especially there was no report on lung cancer . Here we demonstrate that CDA-2 and its main component phenylacetylglutamine ( PG ) reduce the metastatic lung tumor growth , and increases survival time after inoculation with Lewis lung carcinoma ( LLC ) cells in a dose-dependent manner in C57BL6 mice . Proliferative program analysis in cancer cells revealed a fundamental impact of CDA-2 and PG on proliferation and apoptosis , including Bcl-2 , Bcl-XL , cIAP1 , Survivin , PCNA , Ki-67 proteins and TUNEL assays . CDA-2 and PG significantly reduced NF-ÎºB DNA-binding activity in lung cancer cells and in alveolar macrophages of tumor bearing mice and especially decreased the release of inflammatory factors including TNFÎ± , IL-6 , and KC . Furthermore , CDA-2 and PG decrease the expressions of TLR2 , TLR6 , and CD14 , but not TLR1 , TLR3 , TLR4 , and TLR9 in bone-marrow-derived macrophages ( BMDM ) of mice stimulated by LLC-conditioned medium ( LLC-CM ) . Over-expressing TLR2 in BMDM prevented CDA-2 and PG from inhibiting NF-ÎºB activation , as well as induction of TNFÎ± and IL-6 . TLR2:TLR6 complexes mediate the effect of NF-ÎºB inactivation by CDA-2 . In conclusion , CDA-2 potently inhibits lung tumor development by reduction of the inflammation in lung through suppression of NF-ÎºB activation in myeloid cells , associating with modulation of TLR2 signaling .
    OUTPUT:

agent
activating invasion and metastasis;resisting cell death;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: CDA-2 ( cell differentiation agent 2 ) , a urinary preparation , has potent anti- proliferative and pro-apoptotic properties in cancer cells . However , the mechanisms of tumor inhibitory action of CDA-2 are far from clear , and especially there was no report on lung cancer . Here we demonstrate that CDA-2 and its main component phenylacetylglutamine ( PG ) reduce the metastatic lung tumor growth , and increases survival time after inoculation with Lewis lung carcinoma ( LLC ) cells in a dose-dependent manner in C57BL6 mice . Proliferative program analysis in cancer cells revealed a fundamental impact of CDA-2 and PG on proliferation and apoptosis , including Bcl-2 , Bcl-XL , cIAP1 , Survivin , PCNA , Ki-67 proteins and TUNEL assays . CDA-2 and PG significantly reduced NF-ÎºB DNA-binding activity in lung cancer cells and in alveolar macrophages of tumor bearing mice and especially decreased the release of inflammatory factors including TNFÎ± , IL-6 , and KC . Furthermore , CDA-2 and PG decrease the expressions of TLR2 , TLR6 , and CD14 , but not TLR1 , TLR3 , TLR4 , and TLR9 in bone-marrow-derived macrophages ( BMDM ) of mice stimulated by LLC-conditioned medium ( LLC-CM ) . Over-expressing TLR2 in BMDM prevented CDA-2 and PG from inhibiting NF-ÎºB activation , as well as induction of TNFÎ± and IL-6 . TLR2:TLR6 complexes mediate the effect of NF-ÎºB inactivation by CDA-2 . In conclusion , CDA-2 potently inhibits lung tumor development by reduction of the inflammation in lung through suppression of NF-ÎºB activation in myeloid cells , associating with modulation of TLR2 signaling .
    OUTPUT:
