Integrated in silico and experimental methods revealed that Arctigenin inhibited angiogenesis and HCT116 cell migration and invasion through regulating the H1F4A and Wnt/β-catenin pathwayElectronic supplementary information (ESI) available: Table S1 as noted in the detailed information of alternated proteins in the proteome analysis. See DOI: 10.1039/c5mb00439j
Arctigenin (ARG) has been previously reported to exert diverse biological activities including anti-proliferation, anti-inflammatory, and antiviral, etc. In the current study, the anti-metastasis and anti-angiogenesis activities of ARG were investigated. To further understand how ARG played these bi...
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Sprache: | eng |
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Zusammenfassung: | Arctigenin (ARG) has been previously reported to exert diverse biological activities including anti-proliferation, anti-inflammatory, and antiviral,
etc.
In the current study, the anti-metastasis and anti-angiogenesis activities of ARG were investigated. To further understand how ARG played these bioactivities, proteomic approaches were used to profile the proteome changes in response to ARG treatment using 2DE-MS/MS. Using these approaches, a total of 50 differentially expressed proteins were identified and clustered. Bioinformatics analysis suggested that multiple signalling pathways were involved. Moreover, ARG induced anti-metastatic and anti-angiogenesis activities were mainly accompanied by a deactivation of the Wnt/β-catenin pathway in HCT116 cells.
The proteomic analysis integrated signalling network analysis suggested that the Wnt/β-catenin signalling pathway was a novel target of Arctigenin. |
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ISSN: | 1742-206X 1742-2051 |
DOI: | 10.1039/c5mb00439j |