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: OBJECTIVE To study the effect of anandamide ( AEA ) on necrosis in HepG2 cells and to explore the role of AEA in progression of liver cancer . METHODS Localization of the fatty acid hydrolytic enzyme ( FAAH ) , cannabinoid receptors 1(CB1) and cannabinoid receptors 2 ( CB2 ) proteins was detected in L02 and HepG2 cells using immunofluorescence . L02 and HepG2 cells were treated with different concentrations of AEA and methyl-beta-cyclodextrin , and the rates of cells necrosis were examined by PI stain . Meanwhile , the expression levels of FAAH , CB1 and CB2 receptor proteins , as well as P38 mitogen-activated protein kinase ( p-P38 MAPK ) and c-Jun-NH2-terminal kinase ( p-JNK ) proteins , were analyzed by Western blot . RESULTS The FAAH , CB1 and CB2 receptor proteins were observed both in cytoplasm and on membrane in L02 and HepG2 cells . The expression level of FAAH protein was higher in HepG2 than in L02 cells . The expression level of CB1 receptor protein was very low in both L02 and HepG2 cells . The expression level of CB2 receptor protein was high in both L02 and HepG2 cells . AEA treatment induced necrosis in HepG2 cells but not in L02 cells . Methyl-beta-cyclodextrin treatment prevented necrosis in HepG2 cells ( t = 3.702 ; 5.274 ; 3.503 , P less than 0.05 ) . The expression patterns of FAAH , CB1 and CB2 receptor protein in L02 and HepG2 cells were confirmed by western blot , which were consistent with the immunofluorescence results . AEA treatment increased the levels of p-P38MAPK and p-JNK proteins in a dose-dependent manner in HepG2 cells ( F = 11.908 ; 26.054 , P less than 0.05 ) and the increase can be partially by prevented by MCD ( t = 2.801 ; t = 12.829 , P less than 0.05 ) . CONCLUSION AEA treatment induces necrosis in HepG2 cells via CB1 and CB2 receptors and lipid rafts .
    OUTPUT:

agent
resisting cell death;sustaining proliferative signaling
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: OBJECTIVE To study the effect of anandamide ( AEA ) on necrosis in HepG2 cells and to explore the role of AEA in progression of liver cancer . METHODS Localization of the fatty acid hydrolytic enzyme ( FAAH ) , cannabinoid receptors 1(CB1) and cannabinoid receptors 2 ( CB2 ) proteins was detected in L02 and HepG2 cells using immunofluorescence . L02 and HepG2 cells were treated with different concentrations of AEA and methyl-beta-cyclodextrin , and the rates of cells necrosis were examined by PI stain . Meanwhile , the expression levels of FAAH , CB1 and CB2 receptor proteins , as well as P38 mitogen-activated protein kinase ( p-P38 MAPK ) and c-Jun-NH2-terminal kinase ( p-JNK ) proteins , were analyzed by Western blot . RESULTS The FAAH , CB1 and CB2 receptor proteins were observed both in cytoplasm and on membrane in L02 and HepG2 cells . The expression level of FAAH protein was higher in HepG2 than in L02 cells . The expression level of CB1 receptor protein was very low in both L02 and HepG2 cells . The expression level of CB2 receptor protein was high in both L02 and HepG2 cells . AEA treatment induced necrosis in HepG2 cells but not in L02 cells . Methyl-beta-cyclodextrin treatment prevented necrosis in HepG2 cells ( t = 3.702 ; 5.274 ; 3.503 , P less than 0.05 ) . The expression patterns of FAAH , CB1 and CB2 receptor protein in L02 and HepG2 cells were confirmed by western blot , which were consistent with the immunofluorescence results . AEA treatment increased the levels of p-P38MAPK and p-JNK proteins in a dose-dependent manner in HepG2 cells ( F = 11.908 ; 26.054 , P less than 0.05 ) and the increase can be partially by prevented by MCD ( t = 2.801 ; t = 12.829 , P less than 0.05 ) . CONCLUSION AEA treatment induces necrosis in HepG2 cells via CB1 and CB2 receptors and lipid rafts .
    OUTPUT:
