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: The Hippo signaling pathway inhibits cell growth and regulates organ size through a kinase cascade that leads to the phosphorylation and nuclear exclusion of the growth-promoting transcriptional coactivator Yes-associated protein ( YAP)/Yorkie . It mediates contact inhibition of cell growth downstream of cadherin adhesion molecules and other cell surface proteins . Contact inhibition is often antagonized by mitogenic growth factor signaling . We report an important mechanism for this antagonism , inhibition of Hippo pathway signaling by mitogenic growth factors . EGF treatment of immortalized mammary cells triggers the rapid translocation of YAP into the nucleus along with YAP dephosphorylation , both of which depend on Lats , the terminal kinase in the Hippo pathway . A small-molecule inhibitor screen of downstream effector pathways shows that EGF receptor inhibits the Hippo pathway through activation of PI3-kinase ( PI3K ) and phosphoinositide-dependent kinase ( PDK1 ) , but independent of AKT activity . The PI3K-PDK1 pathway also mediates YAP nuclear translocation downstream of lysophosphatidic acid and serum as a result of constitutive oncogenic activation of PI3K . PDK1 associates with the core Hippo pathway-kinase complex through the scaffold protein Salvador . The entire Hippo core complex dissociates in response to EGF signaling in a PI3K-PDK1-dependent manner , leading to inactivation of Lats , dephosphorylation of YAP , and YAP nuclear accumulation and transcriptional activation of its target gene , CTGF . These findings show that an important activity of mitogenic signaling pathways is to inactivate the growth-inhibitory Hippo pathway and provide a mechanism for antagonism between contact inhibition and growth factor action .
    OUTPUT:

agent
sustaining proliferative signaling;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: The Hippo signaling pathway inhibits cell growth and regulates organ size through a kinase cascade that leads to the phosphorylation and nuclear exclusion of the growth-promoting transcriptional coactivator Yes-associated protein ( YAP)/Yorkie . It mediates contact inhibition of cell growth downstream of cadherin adhesion molecules and other cell surface proteins . Contact inhibition is often antagonized by mitogenic growth factor signaling . We report an important mechanism for this antagonism , inhibition of Hippo pathway signaling by mitogenic growth factors . EGF treatment of immortalized mammary cells triggers the rapid translocation of YAP into the nucleus along with YAP dephosphorylation , both of which depend on Lats , the terminal kinase in the Hippo pathway . A small-molecule inhibitor screen of downstream effector pathways shows that EGF receptor inhibits the Hippo pathway through activation of PI3-kinase ( PI3K ) and phosphoinositide-dependent kinase ( PDK1 ) , but independent of AKT activity . The PI3K-PDK1 pathway also mediates YAP nuclear translocation downstream of lysophosphatidic acid and serum as a result of constitutive oncogenic activation of PI3K . PDK1 associates with the core Hippo pathway-kinase complex through the scaffold protein Salvador . The entire Hippo core complex dissociates in response to EGF signaling in a PI3K-PDK1-dependent manner , leading to inactivation of Lats , dephosphorylation of YAP , and YAP nuclear accumulation and transcriptional activation of its target gene , CTGF . These findings show that an important activity of mitogenic signaling pathways is to inactivate the growth-inhibitory Hippo pathway and provide a mechanism for antagonism between contact inhibition and growth factor action .
    OUTPUT:
