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 aim of the present work was to study the expression of the proinflammatory cytokine , interleukin-6 ( IL-6 ) , mediated by bFGF signaling and its possible crosstalk with prostate-specific membrane antigen ( PSMA ) in LNCaP and PC3-PSMA prostate cancer cell lines . PC3 cells stably transfected with PSMA gene were used for restoring PSMA expression . LNCaP and PC3-PSMA cells were exposed to 10ng/mL of basic fibroblast growth factor ( bFGF ) . IL-6 production was measured by ELISA assay , and levels of PSMA expression were assessed by flow cytometry . AKT , ERK1/2 , and p38 phosphorylation were detected by Western blot. bFGF enhances IL-6 production in LNCaP and PC3-PSMA prostate cancer cells . The effect of bFGF on stimulating IL-6 secretion was greater in LNCaP than in PC3-PSMA cells . In the presence of bFGF , PSMA expression was activated after 4days of treatment in LNCaP and PC3-PSMA cells . This activation was not maintained after long term of treatment in both metastatic cell lines . Solely MAPKs pathways ( ERK1/2 and p38 ) were activated after bFGF stimulation in both metastatic cell lines , whereas AKT did not show any activation . The interference of the proinflammatory cytokine , IL-6 , with bFGF signaling and PSMA , should be of high clinical relevance in the treatment of metastatic prostate cancer . In developing novel therapeutic modalities targeting IL-6 , significant attention should be given to PSMA and its inactivation to fight against prostate cancer .
    OUTPUT:

agent
activating invasion and metastasis;tumor promoting inflammation
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 aim of the present work was to study the expression of the proinflammatory cytokine , interleukin-6 ( IL-6 ) , mediated by bFGF signaling and its possible crosstalk with prostate-specific membrane antigen ( PSMA ) in LNCaP and PC3-PSMA prostate cancer cell lines . PC3 cells stably transfected with PSMA gene were used for restoring PSMA expression . LNCaP and PC3-PSMA cells were exposed to 10ng/mL of basic fibroblast growth factor ( bFGF ) . IL-6 production was measured by ELISA assay , and levels of PSMA expression were assessed by flow cytometry . AKT , ERK1/2 , and p38 phosphorylation were detected by Western blot. bFGF enhances IL-6 production in LNCaP and PC3-PSMA prostate cancer cells . The effect of bFGF on stimulating IL-6 secretion was greater in LNCaP than in PC3-PSMA cells . In the presence of bFGF , PSMA expression was activated after 4days of treatment in LNCaP and PC3-PSMA cells . This activation was not maintained after long term of treatment in both metastatic cell lines . Solely MAPKs pathways ( ERK1/2 and p38 ) were activated after bFGF stimulation in both metastatic cell lines , whereas AKT did not show any activation . The interference of the proinflammatory cytokine , IL-6 , with bFGF signaling and PSMA , should be of high clinical relevance in the treatment of metastatic prostate cancer . In developing novel therapeutic modalities targeting IL-6 , significant attention should be given to PSMA and its inactivation to fight against prostate cancer .
    OUTPUT:
