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: That a knock-in mouse harboring a dominant-negative thyroid hormone receptor ( TR)-Î² ( Thrb ) mutation develops metastatic thyroid cancer strongly suggests the involvement of TRÎ² in carcinogenesis . Epigenetic silencing of the THRB gene is common in human cancers . The aim of the present study was to determine how DNA methylation affected the expression of the THRB gene in differentiated thyroid cancer ( DTC ) and how reexpression of the THRB gene attenuated the cancer phenotypes . We used methylation-specific PCR to examine the expression and promoter methylation of the THRB gene in DTC tissues . Thyroid cancer cells with hypermethylated THRB were treated with the demethylating agents 5'-aza-2'-deoxycytidine ( 5'-aza-CdR ) and zebularine to evaluate their impact on the cancer cell phenotypes . THRB mRNA expression in DTC was 90% lower than in normal controls , and this decrease was associated with a higher tumor/lymph node staging . The promoter methylation level of the THRB gene had a significant negative correlation with the expression level of the THRB gene . Treatment of FTC-236 cells with 5'-aza-CdR or zebularine induced reexpression of the THRB gene and inhibited cell proliferation and migration . FTC-236 cells stably expressing TRÎ² exhibited lower cell proliferation and migration through inhibition of Î²-catenin signaling pathways compared with FTC-236 without TRÎ². 5'-Aza-CdR also led to suppression of tumor growth in an in vivo xenograft model using FTC-236 cells consistent with the cell-based studies . These finding indicate that TRÎ² is a tumor suppressor and could be tested as a potential therapeutic target .
    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: That a knock-in mouse harboring a dominant-negative thyroid hormone receptor ( TR)-Î² ( Thrb ) mutation develops metastatic thyroid cancer strongly suggests the involvement of TRÎ² in carcinogenesis . Epigenetic silencing of the THRB gene is common in human cancers . The aim of the present study was to determine how DNA methylation affected the expression of the THRB gene in differentiated thyroid cancer ( DTC ) and how reexpression of the THRB gene attenuated the cancer phenotypes . We used methylation-specific PCR to examine the expression and promoter methylation of the THRB gene in DTC tissues . Thyroid cancer cells with hypermethylated THRB were treated with the demethylating agents 5'-aza-2'-deoxycytidine ( 5'-aza-CdR ) and zebularine to evaluate their impact on the cancer cell phenotypes . THRB mRNA expression in DTC was 90% lower than in normal controls , and this decrease was associated with a higher tumor/lymph node staging . The promoter methylation level of the THRB gene had a significant negative correlation with the expression level of the THRB gene . Treatment of FTC-236 cells with 5'-aza-CdR or zebularine induced reexpression of the THRB gene and inhibited cell proliferation and migration . FTC-236 cells stably expressing TRÎ² exhibited lower cell proliferation and migration through inhibition of Î²-catenin signaling pathways compared with FTC-236 without TRÎ². 5'-Aza-CdR also led to suppression of tumor growth in an in vivo xenograft model using FTC-236 cells consistent with the cell-based studies . These finding indicate that TRÎ² is a tumor suppressor and could be tested as a potential therapeutic target .
    OUTPUT:
