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dc.contributor.authorTsai, Chun-Haoen_US
dc.contributor.authorYang, Ming-Huien_US
dc.contributor.authorHung, Amos C.en_US
dc.contributor.authorWu, Shou-Chengen_US
dc.contributor.authorChiu, Wen-Chinen_US
dc.contributor.authorHou, Ming-Fengen_US
dc.contributor.authorTyan, Yu-Changen_US
dc.contributor.authorWang, Yun-Mingen_US
dc.contributor.authorYuan, Shyng-Shiou F.en_US
dc.date.accessioned2016-03-28T00:04:18Z-
dc.date.available2016-03-28T00:04:18Z-
dc.date.issued2016-01-01en_US
dc.identifier.issn2045-452Xen_US
dc.identifier.urihttp://dx.doi.org/10.1039/c5tx00280jen_US
dc.identifier.urihttp://hdl.handle.net/11536/129520-
dc.description.abstractExposure to arsenic is known to be a risk factor for various types of cancer. Apart from its carcinogenic activity, arsenic also shows promoting effects on angiogenesis, a crucial process for tumor growth. Yet, the mechanism underlying arsenic-induced angiogenesis is not fully understood. In this study, we aimed at investigating the involvement of inhibitor of DNA binding 1 (Id1) and the associated signal molecules in the arsenic-mediated angiogenesis. Our initial screening revealed that treatment with low concentrations of arsenic (0.5-1 mu M) led to multiple cellular responses, including enhanced endothelial cell viability and angiogenic activity as well as increased protein expression of Id1. The arsenic-induced angiogenesis was suppressed in the Id1-knocked down cells compared to that in control cells. Furthermore, arsenic-induced Id1 expression and angiogenic activity were regulated by PI3K/Akt, NF-kappa B, and nitric oxide synthase (NOS) signaling. In summary, our current data demonstrate for the first time that Id1 mediates the arsenic-promoted angiogenesis, and Id1 may be regarded as an antiangiogenesis target for treatment of arsenic-associated cancer.en_US
dc.language.isoen_USen_US
dc.titleIdentification of Id1 as a downstream effector for arsenic-promoted angiogenesis via PI3K/Akt, NF-kappa B and NOS signalingen_US
dc.typeArticleen_US
dc.identifier.doi10.1039/c5tx00280jen_US
dc.identifier.journalTOXICOLOGY RESEARCHen_US
dc.citation.spage151en_US
dc.citation.epage159en_US
dc.contributor.department生物科技學系zh_TW
dc.contributor.department分子醫學與生物工程研究所zh_TW
dc.contributor.departmentDepartment of Biological Science and Technologyen_US
dc.contributor.departmentInstitute of Molecular Medicine and Bioengineeringen_US
dc.identifier.wosnumberWOS:000366832700012en_US
dc.citation.woscount0en_US
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