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: The DNA repair protein Ku70 is a key player in chemoresistance to anticancer agents ( e.g. , etoposide ) or radioresistance . The responses of different organs to radiation vary widely and likely depend on the cell population in the organs . Previously , we established and characterized Ku70-deficient murine lung epithelial ( Ku70 -/- MLE ) cells and found that these cells are more sensitive than Ku70 +/- MLE cells ( control cells ) to X-irradiation , as determined by clonogenic survival assay ; however , the mechanism underlying this sensitivity remains unclear . In this study , we examined the mechanism by which X-irradiation triggers the death of Ku70 -/- MLE cells . Our results showed that Ku70 -/- MLE cells were more sensitive to radiation-induced apoptosis than control cells , although X-irradiation activated caspase-3 and caspase-7 , and cleaved PARP in both cell lines . We also examined the expression level of phosphorylated H2AX ( γH2AX ) , which is a marker of DSB , and observed the phosphorylation of H2AX and the elimination of γH2AX in both cell lines after X-irradiation . The elimination in Ku70 -/- MLE cells was slower than that in control cells , suggesting that DSB repair activity in the Ku70 -/- MLE cells is lower than that in control cells . These findings suggest that Ku70 might play a key role in the inhibition of apoptosis through the DSB repair pathway in lung epithelial cells . Our findings also suggest that these cell lines might be useful for the study of Ku70 functions and the Ku70-dependent DSB repair pathway in lung epithelial cells .
    OUTPUT:

agent
resisting cell death;genomic instability and mutation
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 DNA repair protein Ku70 is a key player in chemoresistance to anticancer agents ( e.g. , etoposide ) or radioresistance . The responses of different organs to radiation vary widely and likely depend on the cell population in the organs . Previously , we established and characterized Ku70-deficient murine lung epithelial ( Ku70 -/- MLE ) cells and found that these cells are more sensitive than Ku70 +/- MLE cells ( control cells ) to X-irradiation , as determined by clonogenic survival assay ; however , the mechanism underlying this sensitivity remains unclear . In this study , we examined the mechanism by which X-irradiation triggers the death of Ku70 -/- MLE cells . Our results showed that Ku70 -/- MLE cells were more sensitive to radiation-induced apoptosis than control cells , although X-irradiation activated caspase-3 and caspase-7 , and cleaved PARP in both cell lines . We also examined the expression level of phosphorylated H2AX ( γH2AX ) , which is a marker of DSB , and observed the phosphorylation of H2AX and the elimination of γH2AX in both cell lines after X-irradiation . The elimination in Ku70 -/- MLE cells was slower than that in control cells , suggesting that DSB repair activity in the Ku70 -/- MLE cells is lower than that in control cells . These findings suggest that Ku70 might play a key role in the inhibition of apoptosis through the DSB repair pathway in lung epithelial cells . Our findings also suggest that these cell lines might be useful for the study of Ku70 functions and the Ku70-dependent DSB repair pathway in lung epithelial cells .
    OUTPUT:
