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.
    ###
    INPUT: p32/gC1qR/C1QBP/HABP1 is a mitochondrial/cell surface protein overexpressed in certain cancer cells . Here we show that knocking down p32 expression in human cancer cells strongly shifts their metabolism from oxidative phosphorylation ( OXPHOS ) to glycolysis . The p32 knockdown cells exhibited reduced synthesis of the mitochondrial-DNA-encoded OXPHOS polypeptides and were less tumorigenic in vivo . Expression of exogenous p32 in the knockdown cells restored the wild-type cellular phenotype and tumorigenicity . Increased glucose consumption and lactate production , known as the Warburg effect , are almost universal hallmarks of solid tumors and are thought to favor tumor growth . However , here we show that a protein regularly overexpressed in some cancers is capable of promoting OXPHOS . Our results indicate that high levels of glycolysis , in the absence of adequate OXPHOS , may not be as beneficial for tumor growth as generally thought and suggest that tumor cells use p32 to regulate the balance between OXPHOS and glycolysis .
    OUTPUT:

agent
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: p32/gC1qR/C1QBP/HABP1 is a mitochondrial/cell surface protein overexpressed in certain cancer cells . Here we show that knocking down p32 expression in human cancer cells strongly shifts their metabolism from oxidative phosphorylation ( OXPHOS ) to glycolysis . The p32 knockdown cells exhibited reduced synthesis of the mitochondrial-DNA-encoded OXPHOS polypeptides and were less tumorigenic in vivo . Expression of exogenous p32 in the knockdown cells restored the wild-type cellular phenotype and tumorigenicity . Increased glucose consumption and lactate production , known as the Warburg effect , are almost universal hallmarks of solid tumors and are thought to favor tumor growth . However , here we show that a protein regularly overexpressed in some cancers is capable of promoting OXPHOS . Our results indicate that high levels of glycolysis , in the absence of adequate OXPHOS , may not be as beneficial for tumor growth as generally thought and suggest that tumor cells use p32 to regulate the balance between OXPHOS and glycolysis .
    OUTPUT:
