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: Autophagy , or autophagocytosis , is a selective intracellular degradative process involving the cell's own lysosomal apparatus . An essential component in cell development , homeostasis , repair and resistance to stress , autophagy may result in either cell death or survival . The targeted region of the cell is sequestered within a membrane structure , the autophagosome , for regulation of the catabolic process . A key factor in both autophagosome formation and autophagosome maturation is a protein encoded by the ultraviolet irradiation resistance-associated gene ( UVRAG ) . Conversely , the serine/threonine-specific protein kinase B ( PKB , also known as Akt ) , which regulates survival in various cancers , inhibits autophagy through mTOR activation . We found that Akt1 may also directly inhibit autophagy by down-regulating UVRAG both in a 293T transient transfection system and breast cancer cells stably expressing Akt1 . The UVRAG with mutations at putative Akt1-phosphorylation sites were still inhibited by Akt1 , and dominant-negative Akt1 also inhibited UVRAG expression , suggesting that Akt1 down-regulates UVRAG by a kinase activity-independent mechanism . We showed that Akt1 overexpression in MDA-MB-231 breast cancer cells down-regulated UVRAG transcription . Cells over-expressing Akt1 were more resistant than control cells to ultraviolet light-induced autophagy and exhibited the associated reduction in cell viability . Levels of the autophagosome indicator protein LC3B-II and mRFP-GFP-LC3 were reduced in cells that over-expressing Akt1 . Inhibiting Akt1 by siRNA or reintroducing UVRAG gene rescued the level of LC3B-II in UV-irradiation . Altogether , these data suggest that Akt1 may inhibit autophagy by decreasing UVRAG expression , which also sensitizes cancer cells to UV irradiation .
    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: Autophagy , or autophagocytosis , is a selective intracellular degradative process involving the cell's own lysosomal apparatus . An essential component in cell development , homeostasis , repair and resistance to stress , autophagy may result in either cell death or survival . The targeted region of the cell is sequestered within a membrane structure , the autophagosome , for regulation of the catabolic process . A key factor in both autophagosome formation and autophagosome maturation is a protein encoded by the ultraviolet irradiation resistance-associated gene ( UVRAG ) . Conversely , the serine/threonine-specific protein kinase B ( PKB , also known as Akt ) , which regulates survival in various cancers , inhibits autophagy through mTOR activation . We found that Akt1 may also directly inhibit autophagy by down-regulating UVRAG both in a 293T transient transfection system and breast cancer cells stably expressing Akt1 . The UVRAG with mutations at putative Akt1-phosphorylation sites were still inhibited by Akt1 , and dominant-negative Akt1 also inhibited UVRAG expression , suggesting that Akt1 down-regulates UVRAG by a kinase activity-independent mechanism . We showed that Akt1 overexpression in MDA-MB-231 breast cancer cells down-regulated UVRAG transcription . Cells over-expressing Akt1 were more resistant than control cells to ultraviolet light-induced autophagy and exhibited the associated reduction in cell viability . Levels of the autophagosome indicator protein LC3B-II and mRFP-GFP-LC3 were reduced in cells that over-expressing Akt1 . Inhibiting Akt1 by siRNA or reintroducing UVRAG gene rescued the level of LC3B-II in UV-irradiation . Altogether , these data suggest that Akt1 may inhibit autophagy by decreasing UVRAG expression , which also sensitizes cancer cells to UV irradiation .
    OUTPUT:
