乳腺癌(BC)是世界上最常见的诊断。甘草素是在甘草属的各种物种中发现的类黄酮,显示抗肿瘤活性。本文旨在探讨甘草素对BC细胞生物学行为的影响及其潜在机制。BC细胞用单独的甘草素处理或在甘草素处理之前用oe-HSP90转染。采用RT-qPCR和Western印迹检测HSP90、Snail、E-cadherin,HSC70和LAMP-2A。细胞活力,扩散,迁移,通过执行MTT评估入侵,菌落形成,划痕,和Transwell分析,分别。甘草素处理降低了HSP90和Snail的水平,增强了E-cadherin的表达并抑制了增殖,迁移,和BC细胞的入侵。此外,甘草素处理降低了HSC70和LAMP-2A的表达,与伴侣介导的自噬(CMA)相关的蛋白质。HSP90过表达促进CMA,入侵,和在甘草素处理下BC细胞的迁移。甘草素抑制HSP90介导的CMA,从而抑制BC细胞生长。
Breast cancer (BC) is most commonly diagnosed worldwide. Liquiritigenin is a flavonoid found in various species of the Glycyrrhiza genus, showing anti-tumor activity. This article was to explore the influences of liquiritigenin on the biological behaviors of BC cells and its underlying mechanism. BC cells were treated with liquiritigenin alone or transfected with oe-HSP90 before liquiritigenin treatment. RT-qPCR and Western blotting were employed to examine the levels of HSP90, Snail, E-cadherin, HSC70, and LAMP-2A. Cell viability, proliferation, migration, and invasion were evaluated by performing MTT, colony formation, scratch, and Transwell assays, respectively. Liquiritigenin treatment reduced HSP90 and Snail levels and enhanced E-cadherin expression as well as inhibiting the proliferation, migration, and invasion of BC cells. Moreover, liquiritigenin treatment decreased the expression of HSC70 and LAMP-2A, proteins related to chaperone-mediated autophagy (CMA). HSP90 overexpression promoted the CMA, invasion, and migration of BC cells under liquiritigenin treatment. Liquiritigenin inhibits HSP90-mediated CMA, thereby suppressing BC cell growth.