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: Dentin matrix protein 1 ( DMP1 ) is a member of the small integrin-binding ligand N-linked glycoprotein ( SIBLING ) family , a group of proteins initially described as mineralized extracellular matrices components . More recently , SIBLINGs have been implicated in several key steps of cancer progression , including angiogenesis . Although proangiogenic activities have been demonstrated for 2 SIBLINGs , the role of DMP1 in angiogenesis has not yet been addressed . We demonstrate that this extracellular matrix protein induced the expression of vascular endothelial cadherin ( VE-cadherin ) , a key regulator of intercellular junctions and contact inhibition of growth of endothelial cells that is also known to modulate vascular endothelial growth factor receptor 2 ( VEGFR-2 ) activity , the major high-affinity receptor for VEGF . DMP1 induced VE-cadherin and p27(Kip1) expression followed by cell-cycle arrest in human umbilical vein endothelial cells ( HUVECs ) in a CD44-dependent manner . VEGF-induced proliferation , migration , and tubulogenesis responses were specifically blocked on DMP1 pretreatment of HUVECs . Indeed , after VE-cadherin induction , DMP1 inhibited VEGFR-2 phosphorylation and Src-mediated signaling . However , DMP1 did not interfere with basic fibroblast growth factor-induced angiogenesis . In vivo , DMP1 significantly reduced laser-induced choroidal neovascularization lesions and tumor-associated angiogenesis . These data enable us to put DMP1 on the angiogenic chessboard for the first time and to identify this protein as a new specific inhibitor of VEGF-induced angiogenesis .
    OUTPUT:

agent
inducing angiogenesis;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: Dentin matrix protein 1 ( DMP1 ) is a member of the small integrin-binding ligand N-linked glycoprotein ( SIBLING ) family , a group of proteins initially described as mineralized extracellular matrices components . More recently , SIBLINGs have been implicated in several key steps of cancer progression , including angiogenesis . Although proangiogenic activities have been demonstrated for 2 SIBLINGs , the role of DMP1 in angiogenesis has not yet been addressed . We demonstrate that this extracellular matrix protein induced the expression of vascular endothelial cadherin ( VE-cadherin ) , a key regulator of intercellular junctions and contact inhibition of growth of endothelial cells that is also known to modulate vascular endothelial growth factor receptor 2 ( VEGFR-2 ) activity , the major high-affinity receptor for VEGF . DMP1 induced VE-cadherin and p27(Kip1) expression followed by cell-cycle arrest in human umbilical vein endothelial cells ( HUVECs ) in a CD44-dependent manner . VEGF-induced proliferation , migration , and tubulogenesis responses were specifically blocked on DMP1 pretreatment of HUVECs . Indeed , after VE-cadherin induction , DMP1 inhibited VEGFR-2 phosphorylation and Src-mediated signaling . However , DMP1 did not interfere with basic fibroblast growth factor-induced angiogenesis . In vivo , DMP1 significantly reduced laser-induced choroidal neovascularization lesions and tumor-associated angiogenesis . These data enable us to put DMP1 on the angiogenic chessboard for the first time and to identify this protein as a new specific inhibitor of VEGF-induced angiogenesis .
    OUTPUT:
