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: MG132 , as a proteasome inhibitor , can induce apoptotic cell death through formation of reactive oxygen species ( ROS ) . In this study , we investigated the effects of MAPK ( MEK , JNK , and p38 ) inhibitors on MG132-treated A549 lung cancer cells in relation to cell growth , cell death , ROS , and glutathione ( GSH ) levels . Treatment with 10 microM MG132 inhibited the growth of A549 cells at 24 h . MG132 also induced apoptosis , which was accompanied by the loss of mitochondrial membrane potential ( MMP ; deltapsi(m) ) . ROS were not increased in MG132-treated A549 cells . MG132 increased GSH-depleted cell numbers and decreased GSH levels . MEK and JNK inhibitors did not strongly affect cell growth , cell death , ROS , and GSH levels in MG132-treated A549 cells . In contrast , p38 inhibitor reduced cell growth inhibition , apoptosis , and MMP ( deltapsi(m) ) loss by MG132 . However , p38 inhibitor did not change ROS level and GSH content . In conclusion , MG132 inhibited the growth of A549 cells via apoptosis without formation of ROS . Treatment with p38 inhibitor rescued some cells from MG132-induced apotposis , which was not affected by ROS and GSH level changes .
    OUTPUT:

agent
resisting cell death;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.
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    INPUT: MG132 , as a proteasome inhibitor , can induce apoptotic cell death through formation of reactive oxygen species ( ROS ) . In this study , we investigated the effects of MAPK ( MEK , JNK , and p38 ) inhibitors on MG132-treated A549 lung cancer cells in relation to cell growth , cell death , ROS , and glutathione ( GSH ) levels . Treatment with 10 microM MG132 inhibited the growth of A549 cells at 24 h . MG132 also induced apoptosis , which was accompanied by the loss of mitochondrial membrane potential ( MMP ; deltapsi(m) ) . ROS were not increased in MG132-treated A549 cells . MG132 increased GSH-depleted cell numbers and decreased GSH levels . MEK and JNK inhibitors did not strongly affect cell growth , cell death , ROS , and GSH levels in MG132-treated A549 cells . In contrast , p38 inhibitor reduced cell growth inhibition , apoptosis , and MMP ( deltapsi(m) ) loss by MG132 . However , p38 inhibitor did not change ROS level and GSH content . In conclusion , MG132 inhibited the growth of A549 cells via apoptosis without formation of ROS . Treatment with p38 inhibitor rescued some cells from MG132-induced apotposis , which was not affected by ROS and GSH level changes .
    OUTPUT:
