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槲皮素通过下调醛脱氢酶 1A1(ALDH1A1)、趋化因子受体 4(CXCR4)、粘蛋白 1(MUC1)和上皮细胞黏附分子(EpCAM)来抑制乳腺癌干细胞。

Quercetin Inhibits Breast Cancer Stem Cells via Downregulation of Aldehyde Dehydrogenase 1A1 (ALDH1A1), Chemokine Receptor Type 4 (CXCR4), Mucin 1 (MUC1), and Epithelial Cell Adhesion Molecule (EpCAM).

机构信息

Key Laboratory of Tropical Biological Resources of Ministry of Education, Department of Pharmacy, College of Marine Science, Hainan University, Haikou, Hainan, China (mainland).

Department of Pharmacognosy, College of Pharmacy, Inner Mongolia Medical University, Hohhot, Inner Mongolia, China (mainland).

出版信息

Med Sci Monit. 2018 Jan 21;24:412-420. doi: 10.12659/msm.908022.

Abstract

BACKGROUND Quercetin, nature's most common flavonoid, possesses anticarcinogenic properties against various forms of cancer. The aim of this study was to investigate the effect of quercetin on breast cancer stem cells in the MDA-MB-231 cell line, and to elucidate the possible mechanisms for those effects. MATERIAL AND METHODS We evaluated breast cancer stem cell proliferation, clone generation, and mammosphere formation to determine the effect of quercetin treatment on breast cancer stem cells. RESULTS In our study, quercetin suppressed breast cancer stem cell proliferation, self-renewal, and invasiveness. It also lowered the expression levels of proteins related to tumorigenesis and cancer progression, such as aldehyde dehydrogenase 1A1, C-X-C chemokine receptor type 4, mucin 1, and epithelial cell adhesion molecules. CONCLUSIONS These results indicate that quercetin targets and destroys breast cancer stem cells, making it a potential novel drug in the fight against cancer.

摘要

背景

槲皮素是自然界最常见的类黄酮之一,具有针对多种癌症的抗癌特性。本研究旨在探讨槲皮素对 MDA-MB-231 细胞系中乳腺癌干细胞的影响,并阐明其作用机制。

材料与方法

我们评估了乳腺癌干细胞的增殖、克隆生成和类球体形成,以确定槲皮素处理对乳腺癌干细胞的影响。

结果

在我们的研究中,槲皮素抑制了乳腺癌干细胞的增殖、自我更新和侵袭。它还降低了与肿瘤发生和癌症进展相关的蛋白的表达水平,如醛脱氢酶 1A1、C-X-C 趋化因子受体 4、粘蛋白 1 和上皮细胞黏附分子。

结论

这些结果表明,槲皮素靶向并破坏乳腺癌干细胞,使其成为抗癌的潜在新型药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd7f/5788241/31b8116ce44d/medscimonit-24-412-g001.jpg

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