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 Wnt/Î²-catenin pathway regulates the viability and radiosensitivity of head and neck squamous cancer cells ( HNSCC ) . Increased Î²-catenin predisposes HNSCC patients to poor prognosis and survival . This study was conducted to determine the mechanism by which Î²-catenin regulates the viability of HNSCC . AMC-HN-3 , -HN-8 , UM-SCC-38 , and -SCC-47 cells , which were established from human head and neck cancer specimens , underwent cell death following Î²-catenin silencing. Î²-Catenin silencing significantly induced G1 arrest and increased the expression of Bax and active caspase-3 , which demonstrates the sequential activation of apoptotic cascades following treatment of HNSCC with targeted siRNA . Intriguingly , Î²-catenin silencing also induced autophagy . Here , we confirm that the number of autophagic vacuoles and the expression of type II light chain 3 were increased in cells that were treated with Î²-catenin siRNA . These cell death modes are most likely due to the activation of LKB1-dependent AMPK following Î²-catenin silencing . The activated LKB1/AMPK pathway in AMC-HN-3 cells caused G1 arrest by phosphorylating p53 and suppressing mTOR signaling . In addition , treating AMC-HN-3 cells with LKB1 siRNA preserved cell viability against Î²-catenin silencing-induced cytotoxicity . Taken together , these results imply that following Î²-catenin silencing , HNSCC undergo both apoptotic and autophagic cell death that are under the control of LKB1/AMPK . To the best of our knowledge , these results suggest for the first time that novel crosstalk between Î²-catenin and the LKB1/AMPK pathway regulates the viability of HNSCC . This study thus presents new insights into our understanding of the cellular and molecular mechanisms involved in Î²-catenin silencing-induced cell death .
    OUTPUT:

agent
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: The Wnt/Î²-catenin pathway regulates the viability and radiosensitivity of head and neck squamous cancer cells ( HNSCC ) . Increased Î²-catenin predisposes HNSCC patients to poor prognosis and survival . This study was conducted to determine the mechanism by which Î²-catenin regulates the viability of HNSCC . AMC-HN-3 , -HN-8 , UM-SCC-38 , and -SCC-47 cells , which were established from human head and neck cancer specimens , underwent cell death following Î²-catenin silencing. Î²-Catenin silencing significantly induced G1 arrest and increased the expression of Bax and active caspase-3 , which demonstrates the sequential activation of apoptotic cascades following treatment of HNSCC with targeted siRNA . Intriguingly , Î²-catenin silencing also induced autophagy . Here , we confirm that the number of autophagic vacuoles and the expression of type II light chain 3 were increased in cells that were treated with Î²-catenin siRNA . These cell death modes are most likely due to the activation of LKB1-dependent AMPK following Î²-catenin silencing . The activated LKB1/AMPK pathway in AMC-HN-3 cells caused G1 arrest by phosphorylating p53 and suppressing mTOR signaling . In addition , treating AMC-HN-3 cells with LKB1 siRNA preserved cell viability against Î²-catenin silencing-induced cytotoxicity . Taken together , these results imply that following Î²-catenin silencing , HNSCC undergo both apoptotic and autophagic cell death that are under the control of LKB1/AMPK . To the best of our knowledge , these results suggest for the first time that novel crosstalk between Î²-catenin and the LKB1/AMPK pathway regulates the viability of HNSCC . This study thus presents new insights into our understanding of the cellular and molecular mechanisms involved in Î²-catenin silencing-induced cell death .
    OUTPUT:
