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 submandibular gland-derived tumor cell line SCA-9 is considered a useful tool to study the signaling pathways involved in proliferation , and their regulation , triggered by different stimuli . It is proposed that the non neuronal cholinergic system : acethylcholine , the enzymes that synthesize and degrade it , and the nicotinic and muscarinic receptors , play a key role in tumorigenesis . Here , we investigate the role of muscarinic receptors in SCA-9 cell proliferation , and the modulation of cholinergic signaling pathways exerted by the nuclear transcription factor ÎºB ( NF-ÎºB ) . The activation of cholinergic receptors by carbachol ( 10â»â¹M ) increased cell proliferation ( P&lt;0.001 ) . This was prevented by preincubating cells with the muscarinic antagonist atropine but not by mecamylamine , a nicotinic receptor blocker . Phospholipase C ( PLC)/nitric oxide synthase ( NOS)/arginase pathway is involved in this effect , since carbachol stimulated nitric oxide production , increased NOS2 and NOS3 expressions , urea production , and arginase II expression ( P&lt;0.001 ) . Also , phospholipase Aâ ( PLAâ)/cyclooxygenase ( COX ) pathway is up-regulated in carbachol-induced SCA-9 cell proliferation , because prostaglandin Eâ liberation ( P&lt;0.001 ) is increased and COX-1 expression is turned up ( P&lt;0.001 ) . Interactions between PLC/NOS/arginases and PLAâ/COX pathways via its metabolites were detected . SCA-9 cells exhibit a constitutive activation of NF-ÎºB , which regulates carbachol-induced NOS2 and 3 , arginase II and COX-1 expressions . In addition , protein kinase C is involved in the up-regulation of NOS2 and arginase II enzymes induced by carbachol via NF-ÎºB . In conclusion , the activation of cholinergic receptors in SCA-9 tumor cells promotes proliferation via muscarinic effector enzymes , and reveals the participation of NF-ÎºB at this step of tumorigenesis .
    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.
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    INPUT: The submandibular gland-derived tumor cell line SCA-9 is considered a useful tool to study the signaling pathways involved in proliferation , and their regulation , triggered by different stimuli . It is proposed that the non neuronal cholinergic system : acethylcholine , the enzymes that synthesize and degrade it , and the nicotinic and muscarinic receptors , play a key role in tumorigenesis . Here , we investigate the role of muscarinic receptors in SCA-9 cell proliferation , and the modulation of cholinergic signaling pathways exerted by the nuclear transcription factor ÎºB ( NF-ÎºB ) . The activation of cholinergic receptors by carbachol ( 10â»â¹M ) increased cell proliferation ( P&lt;0.001 ) . This was prevented by preincubating cells with the muscarinic antagonist atropine but not by mecamylamine , a nicotinic receptor blocker . Phospholipase C ( PLC)/nitric oxide synthase ( NOS)/arginase pathway is involved in this effect , since carbachol stimulated nitric oxide production , increased NOS2 and NOS3 expressions , urea production , and arginase II expression ( P&lt;0.001 ) . Also , phospholipase Aâ ( PLAâ)/cyclooxygenase ( COX ) pathway is up-regulated in carbachol-induced SCA-9 cell proliferation , because prostaglandin Eâ liberation ( P&lt;0.001 ) is increased and COX-1 expression is turned up ( P&lt;0.001 ) . Interactions between PLC/NOS/arginases and PLAâ/COX pathways via its metabolites were detected . SCA-9 cells exhibit a constitutive activation of NF-ÎºB , which regulates carbachol-induced NOS2 and 3 , arginase II and COX-1 expressions . In addition , protein kinase C is involved in the up-regulation of NOS2 and arginase II enzymes induced by carbachol via NF-ÎºB . In conclusion , the activation of cholinergic receptors in SCA-9 tumor cells promotes proliferation via muscarinic effector enzymes , and reveals the participation of NF-ÎºB at this step of tumorigenesis .
    OUTPUT:
