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: We investigated the direct effects of LH-releasing hormone ( LH-RH ) antagonist , Cetrorelix , on the growth of HTOA human epithelial ovarian cancer cell line . RT-PCR revealed the expression of mRNA for LH-RH and its receptor in HTOA cells . Cetrorelix , at concentrations between 10(-9) and 10(-5) M , exerted a dose-dependent antiproliferative action on HTOA cells , as measured by 5-bromo-2'-deoxyuridine incorporation into DNA . Flow cytometric analysis indicated that Cetrorelix , at 10(-5) M , arrested cell cycle in HTOA cells , at G1 phase , after 24 h of treatment . Western blot analysis of cell cycle-regulatory proteins demonstrated that treatment with Cetrorelix ( 10(-5) M ) for 24 h did not change the steady-state levels of cyclin D1 , cyclin E , and cyclin-dependent kinase ( Cdk)4 but decreased the levels of cyclin A and Cdk2 . The protein levels of p21 ( a Cdk inhibitor ) and p53 ( a suppressor of tumor cell growth and a positive regulator for p21 expression ) were increased by Cetrorelix , but the levels of p27 ( a Cdk inhibitor ) did not change significantly . Flow cytometric analysis and terminal deoxynucleotidyltransferase-mediated deoxyuridine 5-triphosphate nick end labeling staining demonstrated that Cetrorelix ( 10(-5) M ) induced apoptosis in HTOA cells . In conclusion , Cetrorelix directly inhibits the proliferation of human epithelial ovarian cancer cells through mechanisms mediated by LH-RH receptor and involving multiple events in cell cycle progression , including G1 phase cell cycle arrest coupled with down-regulation of cyclin A-Cdk2 complex levels , presumably attributable to an up-regulation of p53 and p21 protein levels and apoptosis .
    OUTPUT:

agent
sustaining proliferative signaling;evading growth suppressors;resisting cell death
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: We investigated the direct effects of LH-releasing hormone ( LH-RH ) antagonist , Cetrorelix , on the growth of HTOA human epithelial ovarian cancer cell line . RT-PCR revealed the expression of mRNA for LH-RH and its receptor in HTOA cells . Cetrorelix , at concentrations between 10(-9) and 10(-5) M , exerted a dose-dependent antiproliferative action on HTOA cells , as measured by 5-bromo-2'-deoxyuridine incorporation into DNA . Flow cytometric analysis indicated that Cetrorelix , at 10(-5) M , arrested cell cycle in HTOA cells , at G1 phase , after 24 h of treatment . Western blot analysis of cell cycle-regulatory proteins demonstrated that treatment with Cetrorelix ( 10(-5) M ) for 24 h did not change the steady-state levels of cyclin D1 , cyclin E , and cyclin-dependent kinase ( Cdk)4 but decreased the levels of cyclin A and Cdk2 . The protein levels of p21 ( a Cdk inhibitor ) and p53 ( a suppressor of tumor cell growth and a positive regulator for p21 expression ) were increased by Cetrorelix , but the levels of p27 ( a Cdk inhibitor ) did not change significantly . Flow cytometric analysis and terminal deoxynucleotidyltransferase-mediated deoxyuridine 5-triphosphate nick end labeling staining demonstrated that Cetrorelix ( 10(-5) M ) induced apoptosis in HTOA cells . In conclusion , Cetrorelix directly inhibits the proliferation of human epithelial ovarian cancer cells through mechanisms mediated by LH-RH receptor and involving multiple events in cell cycle progression , including G1 phase cell cycle arrest coupled with down-regulation of cyclin A-Cdk2 complex levels , presumably attributable to an up-regulation of p53 and p21 protein levels and apoptosis .
    OUTPUT:
