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: PURPOSE BMP-6 , which belongs to the TGF-Î² superfamily , is a multifunctional molecule with distinct abilities in embryogenesis and organogenesis . Our recent research has implied that BMP-6 may suppress breast cancer metastasis . In the present study , we extended to elucidate the molecular mechanism by which BMP-6 exerts its anti-tumorigenic effect . METHODS The Boyden chamber assay was used to examine the ability of BMP-6 and HO-1 in MCF-7 malignant progress . RT-PCR , western blot , luciferase assay , and quantitative CHIP were used to determine the potential mechanism and signaling pathways by which BMP-6 and HO-1 function as anti-metastatic factors in MCF-7 cells . RESULTS The Boyden chamber assay showed that BMP-6 inhibited the migration and invasion of MCF-7 cells , which effect was significantly deprived by knockdown of HO-1 . We further demonstrated that BMP-6 treatment resulted in an activation of HO-1 transcription through the recruitment of Smad1/5 to the Smad-responsive element on its promoter . In addition , BMP-6-induced up-regulation of HO-1 exhibited an inhibitory effect on MMP-9 secretion in a paracrine action in MCF-7 cells . Overexpression of BMP-6 and HO-1 synergistically suppressed MMP-9 transcription , which effect was specifically mediated via the MAPK/p38/AP-1 signaling . However , blockade of HO-1 using ZnPPIX totally abolished BMP-6-regulated MMP-9 activation in MCF-7 cells . CONCLUSIONS These observations suggest a novel role of BMP-6/HO-1 cascade to relieve breast cancer metastasis by regulating the secretion of growth factors in tumor microenvironment .
    OUTPUT:

agent
activating invasion and metastasis;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: PURPOSE BMP-6 , which belongs to the TGF-Î² superfamily , is a multifunctional molecule with distinct abilities in embryogenesis and organogenesis . Our recent research has implied that BMP-6 may suppress breast cancer metastasis . In the present study , we extended to elucidate the molecular mechanism by which BMP-6 exerts its anti-tumorigenic effect . METHODS The Boyden chamber assay was used to examine the ability of BMP-6 and HO-1 in MCF-7 malignant progress . RT-PCR , western blot , luciferase assay , and quantitative CHIP were used to determine the potential mechanism and signaling pathways by which BMP-6 and HO-1 function as anti-metastatic factors in MCF-7 cells . RESULTS The Boyden chamber assay showed that BMP-6 inhibited the migration and invasion of MCF-7 cells , which effect was significantly deprived by knockdown of HO-1 . We further demonstrated that BMP-6 treatment resulted in an activation of HO-1 transcription through the recruitment of Smad1/5 to the Smad-responsive element on its promoter . In addition , BMP-6-induced up-regulation of HO-1 exhibited an inhibitory effect on MMP-9 secretion in a paracrine action in MCF-7 cells . Overexpression of BMP-6 and HO-1 synergistically suppressed MMP-9 transcription , which effect was specifically mediated via the MAPK/p38/AP-1 signaling . However , blockade of HO-1 using ZnPPIX totally abolished BMP-6-regulated MMP-9 activation in MCF-7 cells . CONCLUSIONS These observations suggest a novel role of BMP-6/HO-1 cascade to relieve breast cancer metastasis by regulating the secretion of growth factors in tumor microenvironment .
    OUTPUT:
