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: BACKGROUND In this report , we explored the role of PKCalpha and PKCe as mediators of phorbol 12-myristate13-acetate ( PMA)-induced proliferation in pituitary tumor GH3B6 cells , and determined if the ERK1/2 and Akt pathways were activated . METHODS The GH3B6 cell proliferation was estimated by BrdU incorporation and the cell cycle progression by flow cytometric cell cycle analysis . We determined the expression of PKCalpha and PKCe in membrane and cytosolic fractions by western blotting . The subcellular redistribution of both PKC isozymes was analyzed by confocal microscopy . RESULTS Incubation with PMA for 15 min stimulated PKCalpha and PKCe activation , which was correlated with the phosphorylation of ERK1/2 but not Akt . The activation of both these PKC isozymes was closely associated with the stimulation of proliferation and the cell cycle progression induced by PMA in GH3B6 cells , an effect that was blocked by the inhibitors of PKCalpha ( GÃ¶6976 ) and PKCe ( eV1-2 ) . In addition , the pretreatment with the inhibitor of ERK1/2 ( PD98059 ) prevented the mitogenic activity induced by treatment with PMA for 15 min . CONCLUSION We demonstrated that the activation of PKCalpha and PKCe by phorbol ester in tumor pituitary GH3B6 cells led to cell proliferation and cell cycle progression , effects that involved ERK1/2 activation .
    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: BACKGROUND In this report , we explored the role of PKCalpha and PKCe as mediators of phorbol 12-myristate13-acetate ( PMA)-induced proliferation in pituitary tumor GH3B6 cells , and determined if the ERK1/2 and Akt pathways were activated . METHODS The GH3B6 cell proliferation was estimated by BrdU incorporation and the cell cycle progression by flow cytometric cell cycle analysis . We determined the expression of PKCalpha and PKCe in membrane and cytosolic fractions by western blotting . The subcellular redistribution of both PKC isozymes was analyzed by confocal microscopy . RESULTS Incubation with PMA for 15 min stimulated PKCalpha and PKCe activation , which was correlated with the phosphorylation of ERK1/2 but not Akt . The activation of both these PKC isozymes was closely associated with the stimulation of proliferation and the cell cycle progression induced by PMA in GH3B6 cells , an effect that was blocked by the inhibitors of PKCalpha ( GÃ¶6976 ) and PKCe ( eV1-2 ) . In addition , the pretreatment with the inhibitor of ERK1/2 ( PD98059 ) prevented the mitogenic activity induced by treatment with PMA for 15 min . CONCLUSION We demonstrated that the activation of PKCalpha and PKCe by phorbol ester in tumor pituitary GH3B6 cells led to cell proliferation and cell cycle progression , effects that involved ERK1/2 activation .
    OUTPUT:
