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: We previously reported that hepatic stellate cells ( HSCs ) activated by angiotensin II ( AngII ) facilitate stromal fibrosis and tumor progression in intrahepatic cholangiocarcinoma ( ICC ) . AngII has been known as a growth factor which can promote epithelial-to-mesenchymal transition ( EMT ) in renal epithelial cells , alveolar epithelial cells and peritoneal mesothelial cells . However , in the past , the relationship between AngII and stromal cell-derived factor-1 ( SDF-1 ) in the microenvironment around cancer and the role of AngII on EMT of cancer cells has not been reported in detail . SDF-1 and its specific receptor , CXCR4 , are now receiving attention as a mechanism of cell progression and metastasis . In this study , we examined whether activated HSCs promote tumor fibrogenesis , tumor progression and distant metastasis by mediating EMT via the AngII/AngII type 1 receptor ( AT-1 ) and the SDF-1/CXCR4 axis . Two human ICC cell lines and a human HSC line , LI-90 , express CXCR4 . Significantly higher concentration of SDF-1Î± was released into the supernatant of LI-90 cells to which AngII had been added . SDF-1Î± increased the proliferative activity of HSCs and enhanced the activation of HSCs as a growth factor . Furthermore , addition of SDF-1Î± and AngII enhanced the increase of the migratory capability and vimentin expression , reduced E-cadherin expression , and translocated the expression of Î²-catenin into the nucleus and cytoplasm in ICC cells . Co-culture with HSCs also enhanced the migratory capability of ICC cells . These findings suggest that SDF-1Î± , released from activated HSCs and AngII , play important roles in cancer progression , tumor fibrogenesis , and migration in autocrine and paracrine fashion by mediating EMT . Our mechanistic findings may provide pivotal insights into the molecular mechanism of the AngII and SDF-1Î±-initiated signaling pathway that regulates fibrogenesis in cancerous stroma , tumor progression and meta-stasis of tumor cells expressing AT-1 and CXCR4 .
    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: We previously reported that hepatic stellate cells ( HSCs ) activated by angiotensin II ( AngII ) facilitate stromal fibrosis and tumor progression in intrahepatic cholangiocarcinoma ( ICC ) . AngII has been known as a growth factor which can promote epithelial-to-mesenchymal transition ( EMT ) in renal epithelial cells , alveolar epithelial cells and peritoneal mesothelial cells . However , in the past , the relationship between AngII and stromal cell-derived factor-1 ( SDF-1 ) in the microenvironment around cancer and the role of AngII on EMT of cancer cells has not been reported in detail . SDF-1 and its specific receptor , CXCR4 , are now receiving attention as a mechanism of cell progression and metastasis . In this study , we examined whether activated HSCs promote tumor fibrogenesis , tumor progression and distant metastasis by mediating EMT via the AngII/AngII type 1 receptor ( AT-1 ) and the SDF-1/CXCR4 axis . Two human ICC cell lines and a human HSC line , LI-90 , express CXCR4 . Significantly higher concentration of SDF-1Î± was released into the supernatant of LI-90 cells to which AngII had been added . SDF-1Î± increased the proliferative activity of HSCs and enhanced the activation of HSCs as a growth factor . Furthermore , addition of SDF-1Î± and AngII enhanced the increase of the migratory capability and vimentin expression , reduced E-cadherin expression , and translocated the expression of Î²-catenin into the nucleus and cytoplasm in ICC cells . Co-culture with HSCs also enhanced the migratory capability of ICC cells . These findings suggest that SDF-1Î± , released from activated HSCs and AngII , play important roles in cancer progression , tumor fibrogenesis , and migration in autocrine and paracrine fashion by mediating EMT . Our mechanistic findings may provide pivotal insights into the molecular mechanism of the AngII and SDF-1Î±-initiated signaling pathway that regulates fibrogenesis in cancerous stroma , tumor progression and meta-stasis of tumor cells expressing AT-1 and CXCR4 .
    OUTPUT:
