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Mechanism of the anthocyanin single component cyanidin-3-O-glucoside inhibiting proliferation and migration of B16-F10 cells
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- Author:
- No author available
- Journal Title:
- Acta Physiologica Sinica
- Issue:
- 6
- DOI:
- 10.13294/j.aps.2019.0073
- Key Word:
- 矢车菊-3-O-葡萄糖苷;小鼠黑色素瘤B16-F10细胞;增殖;迁移
Abstract： 本研究旨在探讨花青素单一成分矢车菊-3-O-葡萄糖苷(cyanidin-3-O-glucoside,Cy-3-glu)对小鼠黑色素瘤细胞B16-F10增殖和迁移的影响,并阐明相关机理.用不同浓度Cy-3-glu处理B16-F10细胞,采用CCK-8法检测细胞存活率,划痕法检测细胞迁移情况,流式细胞仪检测细胞周期,real-time PCR检测细胞周期相关基因的mRNA表达水平,Western blot检测p-AKT、E-钙黏蛋白(E-cadherin)、N-钙黏蛋白(N-cadherin)和波形蛋白(vimentin)的相对表达水平,并用小动物活体成像仪检测B16-F10细胞在C57BL/6J小鼠体内的生长和迁移情况.结果 显示,Cy-3-glu能明显抑制体外B16-F10细胞的生长(P＜ 0.001)和迁移(P＜0.01),使细胞周期阻滞在S期.Cy-3-glu作用后p-AKT(P＜0.05)、N-cadhefin和vimentin (P＜ 0.001)表达水平显著下降,E-cadherin表达水平升高(P＜0.05).饲喂Cy-3-glu饲料的肿瘤模型C57BL/6J小鼠肿瘤大小和重量显著减小(P＜0.05),肿瘤的转移水平也明显降低.以上结果提示,Cy-3-glu通过抑制PI3K/AKT信号、调节细胞黏附和迁移信号使B16-F10细胞周期停滞在S期,最终抑制其在体内和体外的增殖和迁移.
- [1]R, Doll,R, Peto.The causes of cancer: quantitative estimates of avoidable risks of cancer in the United States today.[J].1981,66(6).
- [2].Epithelial-Mesenchymal Transitions in Development and Disease[J].2009,139(5).
- [3]Tanay Bhatt.Signaling and Mechanical Roles of E-cadherin[J].2013,20(6).
- [4]Amanda, Lassen,Mohammad, Atefi,Lidia, Robert,etc.Effects of AKT inhibitor therapy in response and resistance to BRAF inhibition in melanoma.[J].2014,13.
- [5]Perrone, A.,Masullo, M.,Plaza, A.,etc.Flavone and flavonol glycosides from Astragalus eremophilus and Astragalus vogelii[J].2009,4(1).
- [6]Shu-Ping,Yan,Dan-Xia,Chu,Hai-Feng,Qiu,etc.LncRNA LINC01305 silencing inhibits cell epithelial-mesenchymal transition in cervical cancer by inhibiting TNXB-mediated PI3K/Akt signalling pathway.[J].2019,23(4).
- [7]Lingwei,Liang,Xipeng,Liu,Jieyi,He,etc.Cyanidin-3-glucoside induces mesenchymal to epithelial transition via activating Sirt1 expression in triple negative breast cancer cells.[J].2019,162.
- [8]Damsky,W.E.,Theodosakis,N.,Bosenberg,M..Melanoma metastasis: New concepts and evolving paradigms[J].2014,33(19).
- [9]Larue L,Bellacosa A.Epithelial-mesenchymal transition in development and cancer: role of phosphatidylinositol 3' kinase/AKT pathways.[J].2005,24(50).
- [10]Young-Joon, Surh.Cancer chemoprevention with dietary phytochemicals.[J].2003,3.
- [11]Annalucia, Serafino,Paola, Sinibaldi-Vallebona,Giuseppe, Lazzarino,etc.Differentiation of human melanoma cells induced by cyanidin-3-O-beta-glucopyranoside.[J].2004,18(15).
- [12]Yilmaz M,Christofori G.EMT, the cytoskeleton, and cancer cell invasion.[J].2009,28(1).
- [13]Xia,Li,Junzhou,Wu,Xiaoying,Zhang,etc.Glutathione Reductase-mediated Thiol Oxidative Stress Suppresses Metastasis of Murine Melanoma Cells.[J].2018.
- [14]Niessner H,Flaherty KT,Schittek B,etc.Inhibition of PI3K-AKT-mTOR signaling sensitizes melanoma cells to cisplatin and temozolomide.[J].2009,129(6).
- [15]Niessner, Heike,Schmitz, Jennifer,Tabatabai, Ghazaleh,etc.PI3K Pathway Inhibition Achieves Potent Antitumor Activity in Melanoma Brain Metastases In Vitro and In Vivo[J].2016,22(23).
- [16]Kwong,L.N.,Davies,M.A..Navigating the therapeutic complexity of PI3K pathway inhibition in melanoma[J].2013,19(19).
- [17]Yuxue, Gao,Lihong, Shi,Zhen, Cao,etc.Telocinobufagin inhibits the epithelial-mesenchymal transition of breast cancer cells through the phosphoinositide 3-kinase/protein kinase B/extracellular signal-regulated kinase/Snail signaling pathway.[J].2018,15(5).
- [18]Conrad P,Rimm DL,Jilaveanu LB,etc.Vertical targeting of the phosphatidylinositol-3 kinase pathway as a strategy for treating melanoma.[J].2010,16(24).