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: ABSTRACT : BACKGROUND : The ubiquitin-proteasome system and macroautophagy ( hereafter referred to autophagy ) are two complementary pathways for protein degradation . Emerging evidence suggests that proteasome inhibition might be a promising approach for tumor therapy . Accumulating data suggest that autophagy is activated as a compensatory mechanism upon proteasome activity is impaired . METHOD : Autophagy activation was measured using acridine orange staining and LC3 transition . Cell viability and apoptosis were measured using MTT assay and flow cytometry , respectively . Beclin 1 expression vectors or shRNA against Beclin 1 ( shBeclin 1 ) were transfected to investigate the role of Beclin 1 in autophagy activation and cytotoxicity of ovarian cancer cells induced by proteasome inhibitors . RESULTS : Proteasome inhibitors suppressed proliferation and induced autophagy in ovarian cancer cells . Neither phosphoinositide 3-kinase ( PI3K ) inhibitors nor shRNA against Beclin 1 could abolish the formation of acidic vacuoles and the processing of LC3 induced by proteasome inhibitors . Moreover , Beclin 1 overexpression enhanced anti-proliferative effects of proteasome inhibitors in ovarian cancer cells . CONCLUSIONS : For the first time , the current study demonstrated that proteasome inhibitors induced PI3K and Beclin 1-independent autophagy in ovarian cancer cells . In addition , this study revealed autophagy-independent tumor suppressive effects of Beclin 1 in ovarian cancer cells .
    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.
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    INPUT: ABSTRACT : BACKGROUND : The ubiquitin-proteasome system and macroautophagy ( hereafter referred to autophagy ) are two complementary pathways for protein degradation . Emerging evidence suggests that proteasome inhibition might be a promising approach for tumor therapy . Accumulating data suggest that autophagy is activated as a compensatory mechanism upon proteasome activity is impaired . METHOD : Autophagy activation was measured using acridine orange staining and LC3 transition . Cell viability and apoptosis were measured using MTT assay and flow cytometry , respectively . Beclin 1 expression vectors or shRNA against Beclin 1 ( shBeclin 1 ) were transfected to investigate the role of Beclin 1 in autophagy activation and cytotoxicity of ovarian cancer cells induced by proteasome inhibitors . RESULTS : Proteasome inhibitors suppressed proliferation and induced autophagy in ovarian cancer cells . Neither phosphoinositide 3-kinase ( PI3K ) inhibitors nor shRNA against Beclin 1 could abolish the formation of acidic vacuoles and the processing of LC3 induced by proteasome inhibitors . Moreover , Beclin 1 overexpression enhanced anti-proliferative effects of proteasome inhibitors in ovarian cancer cells . CONCLUSIONS : For the first time , the current study demonstrated that proteasome inhibitors induced PI3K and Beclin 1-independent autophagy in ovarian cancer cells . In addition , this study revealed autophagy-independent tumor suppressive effects of Beclin 1 in ovarian cancer cells .
    OUTPUT:
