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: Inhibition of cell proliferation by fenoterol and fenoterol derivatives in 1321N1 astrocytoma cells is consistent with Î²(2)-adrenergic receptor ( Î²(2)-AR ) stimulation . However , the events that result in fenoterol-mediated control of cell proliferation in other cell types are not clear . Here , we compare the effect of the Î²(2)-AR agonists ( R,R')-fenoterol ( Fen ) and ( R,R')-4-methoxy-1-naphthylfenoterol ( MNF ) on signaling and cell proliferation in HepG2 hepatocarcinoma cells by using Western blotting and [ (3)H]thymidine incorporation assays . Despite the expression of Î²(2)-AR , no cAMP accumulation was observed when cells were stimulated with isoproterenol or Fen , although the treatment elicited both mitogen-activated protein kinase and phosphatidylinositol 3-kinase/Akt activation . Unexpectedly , isoproterenol and Fen promoted HepG2 cell growth , but MNF reduced proliferation together with increased apoptosis . The mitogenic responses of Fen were attenuated by 3-(isopropylamino)-1-[(7-methyl-4-indanyl)oxy]butan-2-ol ( ICI 118,551 ) , a Î²(2)-AR antagonist , whereas those of MNF were unaffected . Because of the coexpression of Î²(2)-AR and cannabinoid receptors ( CBRs ) and their impact on HepG2 cell proliferation , these GÎ±(i)/GÎ±(o)-linked receptors may be implicated in MNF signaling . Cell treatment with ( R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-napthalenylmethanone ( WIN 55,212-2 ) , a synthetic agonist of CB(1)R and CB(2)R , led to growth inhibition , whereas inverse agonists of these receptors blocked MNF mitogenic responses without affecting Fen signaling . MNF responses were sensitive to pertussis toxin . The Î²(2)-AR-deficient U87MG cells were refractory to Fen , but responsive to the antiproliferative actions of MNF and WIN 55,212-2 . The data indicate that the presence of the naphthyl moiety in MNF results in functional coupling to the CBR pathway , providing one of the first examples of a dually acting Î²(2)-AR-CBR ligand .
    OUTPUT:

agent
resisting cell death;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: Inhibition of cell proliferation by fenoterol and fenoterol derivatives in 1321N1 astrocytoma cells is consistent with Î²(2)-adrenergic receptor ( Î²(2)-AR ) stimulation . However , the events that result in fenoterol-mediated control of cell proliferation in other cell types are not clear . Here , we compare the effect of the Î²(2)-AR agonists ( R,R')-fenoterol ( Fen ) and ( R,R')-4-methoxy-1-naphthylfenoterol ( MNF ) on signaling and cell proliferation in HepG2 hepatocarcinoma cells by using Western blotting and [ (3)H]thymidine incorporation assays . Despite the expression of Î²(2)-AR , no cAMP accumulation was observed when cells were stimulated with isoproterenol or Fen , although the treatment elicited both mitogen-activated protein kinase and phosphatidylinositol 3-kinase/Akt activation . Unexpectedly , isoproterenol and Fen promoted HepG2 cell growth , but MNF reduced proliferation together with increased apoptosis . The mitogenic responses of Fen were attenuated by 3-(isopropylamino)-1-[(7-methyl-4-indanyl)oxy]butan-2-ol ( ICI 118,551 ) , a Î²(2)-AR antagonist , whereas those of MNF were unaffected . Because of the coexpression of Î²(2)-AR and cannabinoid receptors ( CBRs ) and their impact on HepG2 cell proliferation , these GÎ±(i)/GÎ±(o)-linked receptors may be implicated in MNF signaling . Cell treatment with ( R)-(+)-[2,3-dihydro-5-methyl-3-(4-morpholinylmethyl)pyrrolo[1,2,3-de]-1,4-benzoxazin-6-yl]-1-napthalenylmethanone ( WIN 55,212-2 ) , a synthetic agonist of CB(1)R and CB(2)R , led to growth inhibition , whereas inverse agonists of these receptors blocked MNF mitogenic responses without affecting Fen signaling . MNF responses were sensitive to pertussis toxin . The Î²(2)-AR-deficient U87MG cells were refractory to Fen , but responsive to the antiproliferative actions of MNF and WIN 55,212-2 . The data indicate that the presence of the naphthyl moiety in MNF results in functional coupling to the CBR pathway , providing one of the first examples of a dually acting Î²(2)-AR-CBR ligand .
    OUTPUT:
