sincalide has been researched along with delphinidin* in 1 studies
1 other study(ies) available for sincalide and delphinidin
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[Delphinidin induces autophagy in HER-2+ breast cancer cells via inhibition of AKT/mTOR pathway].
To explore the effect of delphinidin on breast cancer and the underlying mechanisms. Methods: Human epidermal growth factor receptor-2 (HER-2) positive breast cancer cells MDA-MB-453 were treated by delphinidin. Proliferation of MDA-MB-453 cells was detected by CCK-8 after 48 h. TdT-mediated dUTP nick end labeling (TUNEL) assay and Western blot were used to explore apoptotic status for MDA-MB-453 cells. Fluorescence dot assay, immunofluorescence, and Western blot were used to identify autophagy in breast cancer cells. Results: Delphinidin suppressed proliferation of MDA-MB-453 cells. Delphinidin increased the number of TUNEL positive cells. Delphinidin downregulated the expression of caspase-3 and caspase-9, while upregulated the expression of cleaved caspase-3 and cleaved caspase-9 in a dose-dependent manner. Delphinidin enhanced the number of GFP-LC3 punctate dots, LC3 immunofluorescence dots and the expression of LC3-II and ATG5. Delphinidin inhibited the expression of proteins in mTOR signaling pathway, including AKT, mTOR, eIF4E and p70s6k. Conclusion: Delphinidin induced apoptosis and autophagy by inhibition of AKT/mTOR pathway in HER positive breast cancer cells.. 目的:研究飞燕草素对HER-2+乳腺癌细胞MDA-MB-453自噬的诱导作用及其分子机制。方法:以不同浓度飞燕草素处理MDA-MB-453细胞,CCK-8检测细胞增殖情况;TdT介导的脱氧尿嘧啶缺口末端标记(TdT-mediated dUTP nick end labeling,TUNEL)和Western印迹检测细胞凋亡和与凋亡相关蛋白的表达;荧光斑点、免疫荧光和Western印迹检测自噬的诱导情况和诱导机制。 结果:飞燕草素抑制MDA-MB-453细胞增殖,增加TUNEL阳性细胞数,下调caspase-3 和caspase-9蛋白活性,上调裂解的caspase-3和裂解的caspase-9蛋白活性。飞燕草素增加GFP-LC3荧光斑点数、LC3免疫荧光斑点数、LC3-II和ATG5蛋白表达。飞燕草素下调mTOR通路蛋白AKT,mTOR,eIF4E和p70s6k蛋白活性。结论:飞燕草素诱导HER-2+乳腺癌细胞MDA-MB-453凋亡的同时通过抑制AKT/mTOR通路诱导细胞自噬。. Topics: Anthocyanins; Apoptosis; Autophagy; Biomarkers, Tumor; Breast Neoplasms; Caspase 3; Caspase 9; Cell Line, Tumor; Cell Proliferation; Female; Humans; In Situ Nick-End Labeling; Neoplasm Proteins; Proto-Oncogene Proteins c-akt; Sincalide; TOR Serine-Threonine Kinases | 2017 |