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.
    ###
    INPUT: Growth differentiation factor-15 ( GDF-15 ) and the CCN family member , connective tissue growth factor ( CCN2 ) , are associated with cardiac disease , inflammation and cancer . The precise role and signaling mechanism for these factors in normal and diseased tissues remains elusive . Here we demonstrate an interaction between GDF-15 and CCN2 using yeast two-hybrid assays and have mapped the domain of interaction to the von Willebrand factor type C domain of CCN2 . Biochemical pull down assays using secreted GDF-15 and His-tagged CCN2 produced in PC-3 prostate cancer cells confirmed a direct interaction between these proteins . To investigate the functional consequences of this interaction , in vitro angiogenesis assays were performed . We demonstrate that GDF-15 blocks CCN2-mediated tube formation in human umbilical vein endothelial ( HUVEC ) cells . To examine the molecular mechanism whereby GDF-15 inhibits CCN2-mediated angiogenesis , activation of Î±(V) Î²(3) integrins and focal adhesion kinase ( FAK ) was examined . CCN2-mediated FAK activation was inhibited by GDF-15 and was accompanied by a decrease in Î±(V) Î²(3) integrin clustering in HUVEC cells . These results demonstrate , for the first time , a novel signaling pathway for GDF-15 through interaction with the matricellular signaling molecule CCN2 . Furthermore , antagonism of CCN2 mediated angiogenesis by GDF-15 may provide insight into the functional role of GDF-15 in disease states . J. Cell . Biochem. ï¿½ 2012 Wiley Periodicals , Inc .
    OUTPUT:

agent
inducing angiogenesis
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: Growth differentiation factor-15 ( GDF-15 ) and the CCN family member , connective tissue growth factor ( CCN2 ) , are associated with cardiac disease , inflammation and cancer . The precise role and signaling mechanism for these factors in normal and diseased tissues remains elusive . Here we demonstrate an interaction between GDF-15 and CCN2 using yeast two-hybrid assays and have mapped the domain of interaction to the von Willebrand factor type C domain of CCN2 . Biochemical pull down assays using secreted GDF-15 and His-tagged CCN2 produced in PC-3 prostate cancer cells confirmed a direct interaction between these proteins . To investigate the functional consequences of this interaction , in vitro angiogenesis assays were performed . We demonstrate that GDF-15 blocks CCN2-mediated tube formation in human umbilical vein endothelial ( HUVEC ) cells . To examine the molecular mechanism whereby GDF-15 inhibits CCN2-mediated angiogenesis , activation of Î±(V) Î²(3) integrins and focal adhesion kinase ( FAK ) was examined . CCN2-mediated FAK activation was inhibited by GDF-15 and was accompanied by a decrease in Î±(V) Î²(3) integrin clustering in HUVEC cells . These results demonstrate , for the first time , a novel signaling pathway for GDF-15 through interaction with the matricellular signaling molecule CCN2 . Furthermore , antagonism of CCN2 mediated angiogenesis by GDF-15 may provide insight into the functional role of GDF-15 in disease states . J. Cell . Biochem. ï¿½ 2012 Wiley Periodicals , Inc .
    OUTPUT:
