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 apoptotic effects of interferon lambdas ( IFNÎ»s ) have been described in several types of cancers . However , their effects on human lung cancer cells and the mechanisms are elusive . In addition , the interaction between IFNÎ»s and other interferons remains unclear . The interplay between IFNÎ± and IFNÎ» has been reported . However , although IFNÎ³ is a well-known regulatory interferon , the mechanisms through which it regulates IFNÎ»s in lung cancer cells are unknown . These issues are critical for the application of IFNÎ»s in lung cancer therapy . In this study , we used A549 , a cell line derived from a human lung carcinoma , to characterize the antiproliferative and apoptotic effects of IFNÎ»s on lung cancer , and the interplay between IFNÎ³ and IFNÎ» . Because overexpression of full-length ectopic IFNÎ»R1 led to cell death , we generated A549 cells stably expressing a chimeric receptor ( 10R1/Î»R1 ) , which is composed of the extracellular domain of IL-10 receptor ( IL10R1 ) fused in tandem to the transmembrane and intracellular domains of the IFNÎ» receptor ( IFNÎ»R1 ) . By comparing with A549 cells stably expressing its cognate vector , we demonstrated that IL-10 stimulation triggered the intracellular IFNÎ» signaling via 10R1/Î»R1 receptor . By using A549 cells expressing 10R1/Î»R1 , we report that the IFNÎ»R1 chain of IFNÎ» receptor possesses an intrinsic ability to trigger apoptosis in human lung cancer cells . Although it did not suppress cell proliferation , IFNÎ» signaling via 10R1/Î»R1 receptor induced cell cycle arrest , externalization of phosphatidylserine , DNA fragmentation , activation of caspase-3 , caspase-8 and caspase-9 . However , the caspase inhibitor Z-VAD-FMK did not prevent apoptosis . In addition , the extent of induced apoptosis correlate with the expression levels of the IFNÎ» receptor and the levels of STAT1 activation . Lastly , we demonstrated that IFNÎ³ sensitized A549 cells to IFNÎ»-induced apoptosis , via upregulation of IFNÎ»R1 . These data indicate the potential of IFNÎ» , alone or in combination with IFNÎ³ , in the treatment of human lung carcinoma .
    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 apoptotic effects of interferon lambdas ( IFNÎ»s ) have been described in several types of cancers . However , their effects on human lung cancer cells and the mechanisms are elusive . In addition , the interaction between IFNÎ»s and other interferons remains unclear . The interplay between IFNÎ± and IFNÎ» has been reported . However , although IFNÎ³ is a well-known regulatory interferon , the mechanisms through which it regulates IFNÎ»s in lung cancer cells are unknown . These issues are critical for the application of IFNÎ»s in lung cancer therapy . In this study , we used A549 , a cell line derived from a human lung carcinoma , to characterize the antiproliferative and apoptotic effects of IFNÎ»s on lung cancer , and the interplay between IFNÎ³ and IFNÎ» . Because overexpression of full-length ectopic IFNÎ»R1 led to cell death , we generated A549 cells stably expressing a chimeric receptor ( 10R1/Î»R1 ) , which is composed of the extracellular domain of IL-10 receptor ( IL10R1 ) fused in tandem to the transmembrane and intracellular domains of the IFNÎ» receptor ( IFNÎ»R1 ) . By comparing with A549 cells stably expressing its cognate vector , we demonstrated that IL-10 stimulation triggered the intracellular IFNÎ» signaling via 10R1/Î»R1 receptor . By using A549 cells expressing 10R1/Î»R1 , we report that the IFNÎ»R1 chain of IFNÎ» receptor possesses an intrinsic ability to trigger apoptosis in human lung cancer cells . Although it did not suppress cell proliferation , IFNÎ» signaling via 10R1/Î»R1 receptor induced cell cycle arrest , externalization of phosphatidylserine , DNA fragmentation , activation of caspase-3 , caspase-8 and caspase-9 . However , the caspase inhibitor Z-VAD-FMK did not prevent apoptosis . In addition , the extent of induced apoptosis correlate with the expression levels of the IFNÎ» receptor and the levels of STAT1 activation . Lastly , we demonstrated that IFNÎ³ sensitized A549 cells to IFNÎ»-induced apoptosis , via upregulation of IFNÎ»R1 . These data indicate the potential of IFNÎ» , alone or in combination with IFNÎ³ , in the treatment of human lung carcinoma .
    OUTPUT:
