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: Elevated androgen receptor ( AR ) activity in castration-resistant prostate cancer ( CRPC ) may occur through increased levels of AR coactivator proteins . Vav3 , a guanine nucleotide exchange factor ( GEF ) , is upregulated following progression to castration-resistance in preclinical models and is overexpressed in a significant number of human prostate cancers . Vav3 is a novel coactivator of the AR . We sought to identify Vav3 binding partners in an effort to understand the molecular mechanisms underlying Vav3 enhancement of AR activity and to identify new therapeutic targets . The cell division cycle 37 homolog ( Cdc37 ) , a protein kinase-specific co-chaperone for Hsp90 , was identified as a Vav3 interacting protein by yeast two hybrid screening . Vav3-Cdc37 interaction was confirmed by GST pulldown and , for native proteins , by coimmunoprecipitation experiments in prostate cancer cells . Cdc37 potentiated Vav3 coactivation of AR transcriptional activity and Vav3 enhancement of AR amino-carboxyl terminal ( N-C ) interaction , which is essential for optimal receptor transcriptional activity . Cdc37 increased prostate cancer cell proliferation selectively in Vav3 expressing cells . Cdc37 did not affect Vav3 nucleotide exchange activity , Vav3 protein levels or subcellular localization . Disruption of Vav3-Cdc37 interaction inhibited Vav3 enhancement of AR transcriptional activity and AR N-C interaction . Diminished Vav3-Cdc37 interaction also caused decreased prostate cancer cell proliferation selectively in Vav3 expressing cells . Taken together , we identified a novel Vav3 interacting protein that enhances Vav3 coactivation of AR and prostate cancer cell proliferation . Vav3-Cdc37 interaction may provide a new therapeutic target in prostate cancer .
    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: Elevated androgen receptor ( AR ) activity in castration-resistant prostate cancer ( CRPC ) may occur through increased levels of AR coactivator proteins . Vav3 , a guanine nucleotide exchange factor ( GEF ) , is upregulated following progression to castration-resistance in preclinical models and is overexpressed in a significant number of human prostate cancers . Vav3 is a novel coactivator of the AR . We sought to identify Vav3 binding partners in an effort to understand the molecular mechanisms underlying Vav3 enhancement of AR activity and to identify new therapeutic targets . The cell division cycle 37 homolog ( Cdc37 ) , a protein kinase-specific co-chaperone for Hsp90 , was identified as a Vav3 interacting protein by yeast two hybrid screening . Vav3-Cdc37 interaction was confirmed by GST pulldown and , for native proteins , by coimmunoprecipitation experiments in prostate cancer cells . Cdc37 potentiated Vav3 coactivation of AR transcriptional activity and Vav3 enhancement of AR amino-carboxyl terminal ( N-C ) interaction , which is essential for optimal receptor transcriptional activity . Cdc37 increased prostate cancer cell proliferation selectively in Vav3 expressing cells . Cdc37 did not affect Vav3 nucleotide exchange activity , Vav3 protein levels or subcellular localization . Disruption of Vav3-Cdc37 interaction inhibited Vav3 enhancement of AR transcriptional activity and AR N-C interaction . Diminished Vav3-Cdc37 interaction also caused decreased prostate cancer cell proliferation selectively in Vav3 expressing cells . Taken together , we identified a novel Vav3 interacting protein that enhances Vav3 coactivation of AR and prostate cancer cell proliferation . Vav3-Cdc37 interaction may provide a new therapeutic target in prostate cancer .
    OUTPUT:
