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Vicenin-2 inhibits Wnt/β-catenin signaling and induces apoptosis in HT-29 human colon cancer cell line

Authors Yang D, Zhang X, Zhang W, Rengarajan T

Received 16 August 2017

Accepted for publication 12 March 2018

Published 18 May 2018 Volume 2018:12 Pages 1303—1310

DOI https://doi.org/10.2147/DDDT.S149307

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Qiongyu Guo


Dong Yang,1,* Xiling Zhang,2,* Wencun Zhang,3 Thamaraiselvan Rengarajan4

1Department of Anorectal Surgery, The First People’s Hospital of Lianyungang, Lianyungang, China; 2Department of Anorectal Surgery, Shaanxi Provincial People’s Hospital, Shaanxi, Xi’an, China; 3Department of Anorectal Surgery, The Fourth Hospital of Yu Lin City, Shaanxi Province, China; 4Scigen Research and Innovation, Periyar Technology Business Incubator, Thanjavur, Tamil Nadu, India

*These authors contributed equally to this work

Background: Colorectal cancer (CRC) is among highest prevailing cancers in the whole world, especially in western countries. For a diverse of reasons, patients prefer naturally occurring dietary substances over synthetic agents to prevent cancer. Vicenin-2 is largely available in a medicinal plant Ocimum sanctum and is an apigenin form, 6,8-di-C-glucoside, which has been reported to have a range of pharmacological values which includes antioxidant, hepatoprotective, anti-inflammatory and anti-cancer. This study was aimed to analyze the anti-proliferative effect of Vicenin-2 on human colon cancer cells via the Wnt/β-catenin signaling inhibition.
Methods: MTT assay was used to assess the cell viability at different concentrations and time point. Vicenin-2 at a concentration of 50 μM (IC50) decreased the phosphorylated (inactive) glycogen synthase kinase-3β, cyclin D1, and non-p-β-catenin expressions in HT-29 cells, which were evidenced through western blot analysis.
Results: Further, Vincenin-2 reduced the T-cell factor (TCF) / Leukocyte erythroid factor (LEF) reporter activity in HT-29 cells. Vicenin-2 also promoted substantial cell cycle arrest at the G2M phase of HT-29 cells, as well induced apoptosis in HT-29 cells, as revealed through flow cytometric analysis. Furthermore, immunoblot analysis showed that Vicenin-2 treatment enhanced the expression of Cytochrome C, Bax and caspase-3 whereas suppressed the Bcl-2 expression.
Conclusion: Together, these results revealed that Vicenin-2 can act as a potent inhibitor of HT-29 cell proliferation and can be used as an agent against CRC.

Keywords: colorectal cancer, Vicenin-2, β-catenin, apoptosis, caspase-3

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