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: The aryl hydrocarbon receptor ( AHR ) is a ligand-activated transcription factor that mediates the effects of the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin ( TCDD ) . Recently , AHR has emerged as a potential therapeutic target for breast cancer by virtue of its ability to modulate estrogen receptor-Î± ( ERÎ± ) signalling and/or its ability to block cell proliferation . Our previous studies identified cyclin G2 ( CCNG2 ) , an inhibitor of cell-cycle progression , as an AHR target gene ; however , the mechanism of this regulation is unknown . Chromatin immunoprecipitation assays in T-47D human breast cancer cells revealed a TCDD-dependent recruitment of AHR , nuclear co-activator 3 ( NCoA3 ) and the transcription factor forkhead box A1 ( FOXA1 ) , a key regulator of breast cancer cell signaling , to CCNG2 resulting in increases in CCNG2 mRNA and protein levels . Mutation of the AHR response element ( AHRE ) and forkhead-binding sites abolished TCDD-induced CCNG2-regulated reporter gene activity . RNA interference-mediated knockdown of FOXA1 prevented the TCDD-dependent recruitment of AHR and NCoA3 to CCNG2 and reduced CCNG2 mRNA levels . Interestingly , knockdown of FOXA1 also caused a marked decrease in ERÎ± , but not AHR protein levels . However , RNA interference-mediated knockdown of ERÎ± , a negative regulator of CCNG2 , had no effect on TCDD-dependent AHR or NCoA3 recruitment to or expression of CCNG2 . These findings show that FOXA1 , but not ERÎ± , is essential for AHR-dependent regulation of CCNG2 , assigning a role for FOXA1 in AHR action .
    OUTPUT:

agent
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: The aryl hydrocarbon receptor ( AHR ) is a ligand-activated transcription factor that mediates the effects of the environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin ( TCDD ) . Recently , AHR has emerged as a potential therapeutic target for breast cancer by virtue of its ability to modulate estrogen receptor-Î± ( ERÎ± ) signalling and/or its ability to block cell proliferation . Our previous studies identified cyclin G2 ( CCNG2 ) , an inhibitor of cell-cycle progression , as an AHR target gene ; however , the mechanism of this regulation is unknown . Chromatin immunoprecipitation assays in T-47D human breast cancer cells revealed a TCDD-dependent recruitment of AHR , nuclear co-activator 3 ( NCoA3 ) and the transcription factor forkhead box A1 ( FOXA1 ) , a key regulator of breast cancer cell signaling , to CCNG2 resulting in increases in CCNG2 mRNA and protein levels . Mutation of the AHR response element ( AHRE ) and forkhead-binding sites abolished TCDD-induced CCNG2-regulated reporter gene activity . RNA interference-mediated knockdown of FOXA1 prevented the TCDD-dependent recruitment of AHR and NCoA3 to CCNG2 and reduced CCNG2 mRNA levels . Interestingly , knockdown of FOXA1 also caused a marked decrease in ERÎ± , but not AHR protein levels . However , RNA interference-mediated knockdown of ERÎ± , a negative regulator of CCNG2 , had no effect on TCDD-dependent AHR or NCoA3 recruitment to or expression of CCNG2 . These findings show that FOXA1 , but not ERÎ± , is essential for AHR-dependent regulation of CCNG2 , assigning a role for FOXA1 in AHR action .
    OUTPUT:
