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 anti-apoptotic protein , BAX inhibitor-1 ( BI-1 ) , has a role in cancer/tumor progression . BI-1-overexpressing HT1080 and B16F10 cells produced higher lung weights and tumor volumes after injection into the tail veins of mice . Transfection of BI-1 siRNA into cells before injection blocked lung metastasis. in vitro , the overexpression of BI-1 increased cell mobility and invasiveness , with highly increased glucose consumption and cytosolic accumulation of lactate and pyruvate , but decreased mitochondrial O(2) consumption and ATP production . Glucose metabolism-associated extracellular pH also decreased as cells excreted more H(+) , and sodium hydrogen exchanger ( NHE ) activity increased , probably as a homeostatic mechanism for intracellular pH . These alterations activated MMP 2/9 and cell mobility and invasiveness , which were reversed by the NHE inhibitor , 5-(N-ethyl-N-isopropyl) amiloride ( EIPA ) , suggesting a role for NHE in cancer metastasis . In both in vitro and in vivo experiments , C-terminal deleted ( CDeltaBI-1 ) cells showed similar results to control cells , suggesting that the C-terminal motif is required for BI-1-associated alterations of glucose metabolism , NHE activation and cancer metastasis . These findings strongly suggest that BI-1 reduces extracellular pH and regulates metastasis by altering glucose metabolism and activating NHE , with the C-terminal tail having a pivotal role in these processes .
    OUTPUT:

agent
activating invasion and metastasis;cellular energetics
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 anti-apoptotic protein , BAX inhibitor-1 ( BI-1 ) , has a role in cancer/tumor progression . BI-1-overexpressing HT1080 and B16F10 cells produced higher lung weights and tumor volumes after injection into the tail veins of mice . Transfection of BI-1 siRNA into cells before injection blocked lung metastasis. in vitro , the overexpression of BI-1 increased cell mobility and invasiveness , with highly increased glucose consumption and cytosolic accumulation of lactate and pyruvate , but decreased mitochondrial O(2) consumption and ATP production . Glucose metabolism-associated extracellular pH also decreased as cells excreted more H(+) , and sodium hydrogen exchanger ( NHE ) activity increased , probably as a homeostatic mechanism for intracellular pH . These alterations activated MMP 2/9 and cell mobility and invasiveness , which were reversed by the NHE inhibitor , 5-(N-ethyl-N-isopropyl) amiloride ( EIPA ) , suggesting a role for NHE in cancer metastasis . In both in vitro and in vivo experiments , C-terminal deleted ( CDeltaBI-1 ) cells showed similar results to control cells , suggesting that the C-terminal motif is required for BI-1-associated alterations of glucose metabolism , NHE activation and cancer metastasis . These findings strongly suggest that BI-1 reduces extracellular pH and regulates metastasis by altering glucose metabolism and activating NHE , with the C-terminal tail having a pivotal role in these processes .
    OUTPUT:
