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: Within the family of protein kinase C ( PKC ) molecules , the novel isoform PRKCE ( PKCÉ ) acts as a bona fide oncogene in in vitro and in vivo models of tumorigenesis . Previous studies have reported expression of PKCÉ in breast , prostate and lung tumors above that of normal adjacent tissue . Data from the cancer genome atlas suggest increased copy number of PRKCE in triple negative breast cancer ( TNBC ) . We find that overexpression of PKCÉ in a non-tumorigenic breast epithelial cell line is sufficient to overcome contact inhibition and results in the formation of cellular foci . Correspondingly , inhibition of PKCÉ in a TNBC cell model results in growth defects in two-dimensional ( 2D ) and three-dimensional ( 3D ) culture conditions and orthotopic xenografts . Using stable isotope labeling of amino acids in a cell culture phosphoproteomic approach , we find that CTNND1/p120ctn phosphorylation at serine 268 ( P-S268 ) occurs in a strictly PKCÉ-dependent manner , and that loss of PKCÉ signaling in TNBC cells leads to reversal of mesenchymal morphology and signaling . In a model of Ras activation , inhibition of PKCÉ is sufficient to block mesenchymal cell morphology . Finally , treatment with a PKCÉ ATP mimetic inhibitor , PF-5263555 , recapitulates genetic loss of function experiments impairing p120ctn phosphorylation as well as compromising TNBC cell growth in vitro and in vivo . We demonstrate PKCÉ as a tractable therapeutic target for TNBC , where p120ctn phosphorylation may serve as a readout for monitoring patient response.Oncogene advance online publication , 1 April 2013 ; doi:10.1038/onc.2013.91 .
    OUTPUT:

agent
evading growth suppressors
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: Within the family of protein kinase C ( PKC ) molecules , the novel isoform PRKCE ( PKCÉ ) acts as a bona fide oncogene in in vitro and in vivo models of tumorigenesis . Previous studies have reported expression of PKCÉ in breast , prostate and lung tumors above that of normal adjacent tissue . Data from the cancer genome atlas suggest increased copy number of PRKCE in triple negative breast cancer ( TNBC ) . We find that overexpression of PKCÉ in a non-tumorigenic breast epithelial cell line is sufficient to overcome contact inhibition and results in the formation of cellular foci . Correspondingly , inhibition of PKCÉ in a TNBC cell model results in growth defects in two-dimensional ( 2D ) and three-dimensional ( 3D ) culture conditions and orthotopic xenografts . Using stable isotope labeling of amino acids in a cell culture phosphoproteomic approach , we find that CTNND1/p120ctn phosphorylation at serine 268 ( P-S268 ) occurs in a strictly PKCÉ-dependent manner , and that loss of PKCÉ signaling in TNBC cells leads to reversal of mesenchymal morphology and signaling . In a model of Ras activation , inhibition of PKCÉ is sufficient to block mesenchymal cell morphology . Finally , treatment with a PKCÉ ATP mimetic inhibitor , PF-5263555 , recapitulates genetic loss of function experiments impairing p120ctn phosphorylation as well as compromising TNBC cell growth in vitro and in vivo . We demonstrate PKCÉ as a tractable therapeutic target for TNBC , where p120ctn phosphorylation may serve as a readout for monitoring patient response.Oncogene advance online publication , 1 April 2013 ; doi:10.1038/onc.2013.91 .
    OUTPUT:
