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: Prostaglandin E(2) ( PGE(2) ) receptor subtype EP(2) , which is coupled to cAMP metabolism , is known to mediate proliferation of primary human keratinocytes in vitro . The effect of gain or loss of EP(2) receptors in immortalized human keratinocytes ( HaCat cells ) was examined . HaCat keratinocytes were transfected with sense or anti-sense constructs of the EP(2) receptor . Loss or gain of EP(2) expression was documented by immunoblot and associated changes in agonist-stimulated cAMP production . Loss or gain of EP(2) receptor expression correlated with alterations in plating efficiencies but with modest affects on growth . When cell lines were studied in an organ culture model , anti-sense clones were highly invasive compared with vector controls and sense transfectants . A marked increase in prostaglandin production is commonly seen in malignant lesions . Because prostaglandin receptors are known to undergo ligand-induced receptor down-regulation , we sought to determine whether EP(2) receptor down-regulation results in increased invasiveness . In vector controls , invasiveness was reproduced by ligand-dependent EP(2) receptor down-regulation as assessed by immunohistochemistry . In addition , loss of EP(2) receptor expression was associated with decreased paxillin expression , a critical component of focal adhesion assembly . Thus , down-regulation of EP(2) receptors represents a potential mechanism for neoplastic progression to an invasive phenotype .
    OUTPUT:

agent
activating invasion and metastasis;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.
    ###
    INPUT: Prostaglandin E(2) ( PGE(2) ) receptor subtype EP(2) , which is coupled to cAMP metabolism , is known to mediate proliferation of primary human keratinocytes in vitro . The effect of gain or loss of EP(2) receptors in immortalized human keratinocytes ( HaCat cells ) was examined . HaCat keratinocytes were transfected with sense or anti-sense constructs of the EP(2) receptor . Loss or gain of EP(2) expression was documented by immunoblot and associated changes in agonist-stimulated cAMP production . Loss or gain of EP(2) receptor expression correlated with alterations in plating efficiencies but with modest affects on growth . When cell lines were studied in an organ culture model , anti-sense clones were highly invasive compared with vector controls and sense transfectants . A marked increase in prostaglandin production is commonly seen in malignant lesions . Because prostaglandin receptors are known to undergo ligand-induced receptor down-regulation , we sought to determine whether EP(2) receptor down-regulation results in increased invasiveness . In vector controls , invasiveness was reproduced by ligand-dependent EP(2) receptor down-regulation as assessed by immunohistochemistry . In addition , loss of EP(2) receptor expression was associated with decreased paxillin expression , a critical component of focal adhesion assembly . Thus , down-regulation of EP(2) receptors represents a potential mechanism for neoplastic progression to an invasive phenotype .
    OUTPUT:
