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: Tumour cells primarily utilize aerobic glycolysis for energy production , a phenomenon known as the Warburg effect . Its mechanism is not well understood . The tumour suppressor gene p53 is frequently mutated in tumours . Many tumour-associated mutant p53 ( mutp53 ) proteins not only lose tumour suppressive function but also gain new oncogenic functions that are independent of wild-type p53 , defined as mutp53 gain of function ( GOF ) . Here we show that tumour-associated mutp53 stimulates the Warburg effect in cultured cells and mutp53 knockin mice as a new mutp53 GOF . Mutp53 stimulates the Warburg effect through promoting GLUT1 translocation to the plasma membrane , which is mediated by activated RhoA and its downstream effector ROCK . Inhibition of RhoA/ROCK/GLUT1 signalling largely abolishes mutp53 GOF in stimulating the Warburg effect . Furthermore , inhibition of glycolysis in tumour cells greatly compromises mutp53 GOF in promoting tumorigenesis . Thus , our results reveal a new mutp53 GOF and a mechanism for controlling the Warburg effect .
    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: Tumour cells primarily utilize aerobic glycolysis for energy production , a phenomenon known as the Warburg effect . Its mechanism is not well understood . The tumour suppressor gene p53 is frequently mutated in tumours . Many tumour-associated mutant p53 ( mutp53 ) proteins not only lose tumour suppressive function but also gain new oncogenic functions that are independent of wild-type p53 , defined as mutp53 gain of function ( GOF ) . Here we show that tumour-associated mutp53 stimulates the Warburg effect in cultured cells and mutp53 knockin mice as a new mutp53 GOF . Mutp53 stimulates the Warburg effect through promoting GLUT1 translocation to the plasma membrane , which is mediated by activated RhoA and its downstream effector ROCK . Inhibition of RhoA/ROCK/GLUT1 signalling largely abolishes mutp53 GOF in stimulating the Warburg effect . Furthermore , inhibition of glycolysis in tumour cells greatly compromises mutp53 GOF in promoting tumorigenesis . Thus , our results reveal a new mutp53 GOF and a mechanism for controlling the Warburg effect .
    OUTPUT:
