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: Mitochondrial uncoupling protein 2 ( UCP2 ) can moderate oxidative stress by favoring the influx of protons into the mitochondrial matrix , thus reducing electron leakage from respiratory chain and mitochondrial superoxide production . Here , we demonstrate that UCP2 inhibition by genipin or UCP2 siRNA strongly increases reactive oxygen species ( ROS ) production inhibiting pancreatic adenocarcinoma cell growth . We also show that UCP2 inhibition triggers ROS-dependent nuclear translocation of the glycolytic enzyme glyceraldehyde 3-phosphate dehydrogenase ( GAPDH ) , formation of autophagosomes , and the expression of the autophagy marker LC3-II . Consistently , UCP2 over-expression significantly reduces basal autophagy confirming the anti-autophagic role of UCP2 . Furthermore , we demonstrate that autophagy induced by UCP2 inhibition determines a ROS-dependent cell death , as indicated by the apoptosis decrease in the presence of the autophagy inhibitors chloroquine ( CQ ) or 3-methyladenine ( 3-MA ) , or the radical scavenger NAC . Intriguingly , the autophagy induced by genipin is able to potentiate the autophagic cell death triggered by gemcitabine , the standard chemotherapeutic drug for pancreatic adenocarcinoma , supporting the development of an anti-cancer therapy based on UCP2 inhibition associated to standard chemotherapy . Our results demonstrate for the first time that UCP2 plays a role in autophagy regulation bringing new insights into mitochondrial uncoupling protein field .
    OUTPUT:

agent
tumor promoting inflammation;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: Mitochondrial uncoupling protein 2 ( UCP2 ) can moderate oxidative stress by favoring the influx of protons into the mitochondrial matrix , thus reducing electron leakage from respiratory chain and mitochondrial superoxide production . Here , we demonstrate that UCP2 inhibition by genipin or UCP2 siRNA strongly increases reactive oxygen species ( ROS ) production inhibiting pancreatic adenocarcinoma cell growth . We also show that UCP2 inhibition triggers ROS-dependent nuclear translocation of the glycolytic enzyme glyceraldehyde 3-phosphate dehydrogenase ( GAPDH ) , formation of autophagosomes , and the expression of the autophagy marker LC3-II . Consistently , UCP2 over-expression significantly reduces basal autophagy confirming the anti-autophagic role of UCP2 . Furthermore , we demonstrate that autophagy induced by UCP2 inhibition determines a ROS-dependent cell death , as indicated by the apoptosis decrease in the presence of the autophagy inhibitors chloroquine ( CQ ) or 3-methyladenine ( 3-MA ) , or the radical scavenger NAC . Intriguingly , the autophagy induced by genipin is able to potentiate the autophagic cell death triggered by gemcitabine , the standard chemotherapeutic drug for pancreatic adenocarcinoma , supporting the development of an anti-cancer therapy based on UCP2 inhibition associated to standard chemotherapy . Our results demonstrate for the first time that UCP2 plays a role in autophagy regulation bringing new insights into mitochondrial uncoupling protein field .
    OUTPUT:
