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: Hepatocyte growth factor ( HGF ) , a mesenchymal-derived factor which regulates growth , motility , and morphogenesis of epithelial and endothelial cells , functions as a hepatotrophic and renotrophic factor for regeneration of the liver and kidney . We have now obtained evidence that transforming growth factor-beta 1 ( TGF-beta 1 ) and glucocorticoids are negative regulators for HGF gene expression . When TGF-beta 1 or dexamethasone was added to cultures of MRC-5 human embryonic lung fibroblasts and HL-60 human promyelocytic leukemic cells , the amount of HGF secreted into the culture medium was inhibited to 30-40% of that of control cultures by 10 ng/ml TGF-beta 1 and to 40-50% by 10(-6) M dexamethasone . The inhibitory effect of TGF-beta 1 and dexamethasone on HGF synthesis in MRC-5 cells was additive , thereby suggesting that TGF-beta 1 and dexamethasone exert effects through distinct mechanisms . Hydrocortisone also inhibited HGF synthesis with the same potency as dexamethasone ; however , testosterone , estriol , and beta-estradiol had no effect . The rate of HGF synthesis in MRC-5 cells , as measured by pulse labeling with [ 35S]methionine and subsequent immunoprecipitation , was suppressed to 30-40% of the control with 10 ng/ml TGF-beta 1 , and to 30-45% by 10(-6) M dexamethasone . HGF mRNA levels in MRC-5 cells and HL-60 cells were dose-dependently suppressed by TGF-beta 1 and dexamethasone ; 10 ng/ml TGF-beta 1 suppressed HGF mRNA levels to 32% and 35% of control culture , respectively , in MRC-5 cells and HL-60 cells , and 10(-6) M dexamethasone suppressed to 43% and 38% , respectively . Thus , TGF-beta 1 and glucocorticoids seem to inhibit HGF synthesis by suppressing the expression of the HGF gene . We propose that a negative regulation of HGF gene expression by TGF-beta 1 or glucocorticoids may be involved in physiological or pathological processes during tissue regeneration .
    OUTPUT:

agent
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.
    ###
    INPUT: Hepatocyte growth factor ( HGF ) , a mesenchymal-derived factor which regulates growth , motility , and morphogenesis of epithelial and endothelial cells , functions as a hepatotrophic and renotrophic factor for regeneration of the liver and kidney . We have now obtained evidence that transforming growth factor-beta 1 ( TGF-beta 1 ) and glucocorticoids are negative regulators for HGF gene expression . When TGF-beta 1 or dexamethasone was added to cultures of MRC-5 human embryonic lung fibroblasts and HL-60 human promyelocytic leukemic cells , the amount of HGF secreted into the culture medium was inhibited to 30-40% of that of control cultures by 10 ng/ml TGF-beta 1 and to 40-50% by 10(-6) M dexamethasone . The inhibitory effect of TGF-beta 1 and dexamethasone on HGF synthesis in MRC-5 cells was additive , thereby suggesting that TGF-beta 1 and dexamethasone exert effects through distinct mechanisms . Hydrocortisone also inhibited HGF synthesis with the same potency as dexamethasone ; however , testosterone , estriol , and beta-estradiol had no effect . The rate of HGF synthesis in MRC-5 cells , as measured by pulse labeling with [ 35S]methionine and subsequent immunoprecipitation , was suppressed to 30-40% of the control with 10 ng/ml TGF-beta 1 , and to 30-45% by 10(-6) M dexamethasone . HGF mRNA levels in MRC-5 cells and HL-60 cells were dose-dependently suppressed by TGF-beta 1 and dexamethasone ; 10 ng/ml TGF-beta 1 suppressed HGF mRNA levels to 32% and 35% of control culture , respectively , in MRC-5 cells and HL-60 cells , and 10(-6) M dexamethasone suppressed to 43% and 38% , respectively . Thus , TGF-beta 1 and glucocorticoids seem to inhibit HGF synthesis by suppressing the expression of the HGF gene . We propose that a negative regulation of HGF gene expression by TGF-beta 1 or glucocorticoids may be involved in physiological or pathological processes during tissue regeneration .
    OUTPUT:
