首页|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

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

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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.
PrxⅠRegulates Apoptosis of Triple Negative Breast Cancer Cells by Mediating ROS and Mitochondrial Damage
It aimed to elucidate the killing effect of Erastin on triple negative breast cancer cells and the related regulatory mechanism of Prx Ⅰ on triple negative breast cancer MDA-MB-231 cells.The effects of knock-down Prx Ⅰ on 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 Prx Ⅰ could 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 Prx Ⅰ knock-down,indicating that autophagy was activated by ERK after Prx Ⅰ knock-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 Prx Ⅰ preparation.

Triple negative breast cancerPrxⅠROSmitochondrial damageautophagy

马大宇、练旭冬、李浩然、吕树旗、姜鹏、孙率洋、韩英浩

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黑龙江八一农垦大学生命科学技术学院,大庆 163319

三阴性乳腺癌 PrxⅠ 活性氧 线粒体损伤 自噬

黑龙江省自然基金项目

LH2021C061

2024

黑龙江八一农垦大学学报
黑龙江八一农垦大学

黑龙江八一农垦大学学报

影响因子:0.888
ISSN:1002-2090
年,卷(期):2024.36(4)