PrxⅠ通过介导ROS以及线粒体损伤调控三阴性乳腺癌细胞凋亡

PrxⅠRegulates Apoptosis of Triple Negative Breast Cancer Cells by Mediating ROS and Mitochondrial Damage

旨在阐述Erastin对三阴性乳腺癌细胞的杀伤作用,并且阐述了PrxⅠ在其中对三阴性乳腺癌MDA-MB-231细胞的相关调控机制。以细胞实验为主,分别采用免疫荧光、Western Blot和MTT等方法检测敲降PrxⅠ对MDA-MB-231细胞内ROS、线粒体损伤和细胞死亡情况的影响。结果表明:敲降PrxⅠ能够引起细胞内大量产生ROS以及线粒体损伤。同时,在PrxⅠ敲降后调控自噬相关蛋白ERK蛋白表达水平明显升高,表明PrxⅠ敲降后通过ERK激活自噬。最终阐述了调控人三阴性乳腺癌MDA-MB-231细胞死亡的方式,为治疗三阴性乳腺癌提供新思路,为PrxⅠ制剂临床应用提供理论依据。

It aimed to elucidate the killing effect of Erastin on triple negative breast cancer cells and the related regulatory mechanism of PrxⅠon triple negative breast cancer MDA-MB-231 cells.The effects of knock-down PrxⅠon ROS,mitochondrial damage and cell death in MDA-MB-231 cells were detected by immunofluorescence,Western Blot and MTT,respectively.The results showed that knockdown PrxⅠcould induce a large amount of ROS production and mitochondrial damage in the cell.At the same time,the expression level of autophagy related protein ERK was significantly increased after PrxⅠknock-down,indicating that autophagy was activated by ERK after PrxⅠknock-down.Finally,the regulation of MDA-MB-231 cell death in human triple-negative breast cancer is described,which provided a new idea for the treatment of triple-negative breast cancer and a theoretical basis for the clinical application of PrxⅠpreparation.