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: E6-associated protein ( E6-AP ) is a dual function protein . It acts as an E3 ubiquitin-protein ligase enzyme and coactivator of steroid hormone receptors such as estrogen ( ERÎ± ) and progesterone ( PR ) receptors . It promotes the degradation of ERÎ± and PR through the ubiquitin-proteasome pathway . Furthermore , it has been shown that the levels of E6-AP are inversely associated with that of ERÎ± in human breast tumors . But the role of wild-type human E6-AP and its ubiquitin-protein ligase activity in mammary tumorigenesis is still unknown . To investigate this role , the authors utilized transgenic mice lines that specifically overexpress either the wild-type human E6-AP ( E6-AP(WT) ) or the ubiquitin-protein ligase defective E6-AP that contains C833S mutation ( E6-AP(C833S) ) in the mammary gland . To further substantiate the role of E6-AP in the development of breast tumorigenesis , it was also examined the expression of E6-AP in a large cohort of human breast cancer samples . The transgenic mice that overexpress wild-type E6-AP ( E6-AP(WT) ) fail to develop mammary tumors . Unlike the E6-AP(WT) mice , the E6-AP(C833S) mice that overexpress ubiquitin-protein ligase defective E6-AP protein develop mammary hyperplasia with a median latency of 18months . These observations suggest that the inactivation of the ubiquitin-protein ligase function of E6-AP is sufficient to initiate the process of mammary tumor development . Furthermore , the data also suggests that E6-AP exerts its effects on target cells by modulating the protein levels and functions of ERÎ± and PR . In addition , it was found in human breast cancer patients that the level of E6-AP is decreased in invasive breast tumors compared to normal breast tissue . Moreover , the authors also show that the survival patterns for E6-AP negative patients were worse compared to E6-AP positive patients . Taken together , these data suggests that E6-AP may act as a tumor suppressor in breast .
    OUTPUT:

agent
activating invasion and metastasis
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: E6-associated protein ( E6-AP ) is a dual function protein . It acts as an E3 ubiquitin-protein ligase enzyme and coactivator of steroid hormone receptors such as estrogen ( ERÎ± ) and progesterone ( PR ) receptors . It promotes the degradation of ERÎ± and PR through the ubiquitin-proteasome pathway . Furthermore , it has been shown that the levels of E6-AP are inversely associated with that of ERÎ± in human breast tumors . But the role of wild-type human E6-AP and its ubiquitin-protein ligase activity in mammary tumorigenesis is still unknown . To investigate this role , the authors utilized transgenic mice lines that specifically overexpress either the wild-type human E6-AP ( E6-AP(WT) ) or the ubiquitin-protein ligase defective E6-AP that contains C833S mutation ( E6-AP(C833S) ) in the mammary gland . To further substantiate the role of E6-AP in the development of breast tumorigenesis , it was also examined the expression of E6-AP in a large cohort of human breast cancer samples . The transgenic mice that overexpress wild-type E6-AP ( E6-AP(WT) ) fail to develop mammary tumors . Unlike the E6-AP(WT) mice , the E6-AP(C833S) mice that overexpress ubiquitin-protein ligase defective E6-AP protein develop mammary hyperplasia with a median latency of 18months . These observations suggest that the inactivation of the ubiquitin-protein ligase function of E6-AP is sufficient to initiate the process of mammary tumor development . Furthermore , the data also suggests that E6-AP exerts its effects on target cells by modulating the protein levels and functions of ERÎ± and PR . In addition , it was found in human breast cancer patients that the level of E6-AP is decreased in invasive breast tumors compared to normal breast tissue . Moreover , the authors also show that the survival patterns for E6-AP negative patients were worse compared to E6-AP positive patients . Taken together , these data suggests that E6-AP may act as a tumor suppressor in breast .
    OUTPUT:
