Study on the Molecular Mechanism of Endometrial Fibrosis Mediated by Oxidative Stress Injury in Breast Cancer
we used the MDA-MB-231 breast cancer cell line to construct a breast tumor xenograft mouse model, and compared the volume and weight of the uterus of mice in the normal group with those of mice in the tumor group, and found that the uterine body of the tumor group became thinner and narrower, suggesting that the uterine tissue of the tumor group was subjected to certain pathological damage changes. By transcriptome sequencing analysis, it was found that the differential genes focused on fibrosis-related pathways, oxidative stress function, oxidative phosphorylation (OXPHOS), mitochondrial ATP synthesis and so on. By means of immunohistochemical staining of uterine tissues and various molecular experiments to detect the degree of fibrosis in the endometrium, it was found that the endometrium of mice in the tumor group produced fibrotic deposition and the thickness of the endometrium became thinner compared with that of mice in the normal group. Meanwhile, SOD, GSH and MDA tests revealed that antioxidant enzymes were reduced, oxidation products were increased, ROS aggregation occurred and oxidative stress was generated in the tumor group mice. Excessive ROS caused changes in the microenvironment, activated the TGFß-p38MAPK pathway, and led to phosphorylation of p38 protein, which triggered the Epithelial-Mesenchymal Transition (EMT) reaction in the endometrium, resulting in endometrial fibrosis. Overall design: Comparative gene expression profiling analysis of RNA-seq data for endometrium of normal mice and breast cancer tumor mice.