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

Abstract

BackgroundColorectal 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.MethodsMTT 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.ResultsFurther, 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.ConclusionTogether, 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.

Destruxin B Suppresses Drug-Resistant Colon Tumorigenesis and Stemness Is Associated with the Upregulation of miR-214 and Downregulation of mTOR/β-Catenin Pathway

“…Here, we showed that DB treatment not only suppressed colon tumorigenesis, but also CSC phenotypes. DB-medicated CSC-inhibitory effects were associated with the decreased expression of the IGF downstream oncogenic marker, mTOR/STAT3, as well as the stemness marker, β-catenin, both of which have been reported to contribute to treatment failure and the recurrence of colon cancer [ 23 , 34 , 35 ].…”

Role of Wnt/β-Catenin Signaling in the Chemoresistance Modulation of Colorectal Cancer

“…Lastly, apoptosis-related proteins showed significant roles in regulating chemoresistance. Yang et al [29] reported that Vicenin-2 induces apoptosis in colon cancer by suppressing Bcl-2 and enhancing the expression of Bax and caspase-3 through Wnt/β-catenin signaling. Li et al [30] demonstrated that silencing aquaporin-5 could enhance the sensitivity of CRC cells to 5-FU by inducing apoptosis through the Wnt/β-catenin signaling pathway.…”

Structure Identification of ViceninII Extracted from Dendrobium officinale and the Reversal of TGF-β1-Induced Epithelial–Mesenchymal Transition in Lung Adenocarcinoma Cells through TGF-β/Smad and PI3K/Akt/mTOR Signaling Pathways

“…ViceninII, or 6,8-di-C-glucoside of apigenin, a nontoxic flavonoid that was originally identified from Vitex lucens wood and that is present in many plant sources in Southern Asia, such as Dendrobium officinale , Urtica circularis , Lychnophora and other species [40,41,42], is an effective anti-inflammatory [43,44,45,46], antiglycation [47], anti-spasmodic [48], antiseptic [49], antithrombotic, and antiplatelet agent [50]. ViceninII exhibits significant anticancer activities that inhibit the growth of prostate cancer (PC-3, DU-145 and LNCaP cells) in-vitro and in-vivo [51,52] and induce apoptosis in hT-29 human colon cancer cells [53]. In addition, many critical literatures has been reported that ViceninII has shown anti-inflammatory effect through the inhibition of TGF-β-induced protein signaling pathway as well as induced apoptosis of lung cancer H23 cell via PI3K/Akt/mTOR signaling [54,55].…”