Astragaloside IV (AS-IV) alleviates the malignant biological behavior of hepatocellular carcinoma via Wnt/β-catenin signaling pathway
Astragaloside IV (AS-IV) is an active substance isolated from Astragalus membranaceus (Fisch.) Bungede, which has been shown to have pharmacological effects in a variety of cancers. However, the effects of AS-IV in hepatocellular carcinoma (HCC) and its related mechanisms have been poorly understood...
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Published in | RSC advances Vol. 9; no. 61; pp. 35473 - 35482 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
England
Royal Society of Chemistry
01.11.2019
The Royal Society of Chemistry |
Subjects | |
Online Access | Get full text |
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Summary: | Astragaloside IV (AS-IV) is an active substance isolated from
Astragalus membranaceus
(Fisch.) Bungede, which has been shown to have pharmacological effects in a variety of cancers. However, the effects of AS-IV in hepatocellular carcinoma (HCC) and its related mechanisms have been poorly understood. In this study, we explored the roles of AS-IV on HCC and the underlying signaling pathway. We reported that the appropriate concentrations of AS-IV (25, 50, 100 nmol l
−1
) significantly suppressed the proliferation and cell cycle of HepG2 and Hep3B cell lines whilst promoting apoptosis. Besides, a trans-well and wound healing assay showed that AS-IV could markedly inhibit the migration and invasion of HepG2 and Hep3B cells, the expression of E-cadherin was up-regulation but the expression of N-cadherin and vimentin was down-regulation, and the protein levels of cleaved-caspase-3, 9 were increased markedly compared with the corresponding control. Furthermore, animal model treatment revealed that AS-IV could effectively reduce tumor formation. Moreover, AS-IV also significantly weakened the expression of Wnt, β-catenin and TCF-4
in vitro
and
in vivo
. Taken together, these results suggested that AS-IV inhibited the biological processes of HCC
via
regulating of the Wnt/β-catenin pathway. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 ObjectType-Correction/Retraction-3 |
ISSN: | 2046-2069 2046-2069 |
DOI: | 10.1039/C9RA05933D |