{"title":"MiR-519e-5p regulates malignant phenotype of breast cancer cells through binding to CTPS1","authors":"","doi":"10.1016/j.yexcr.2024.114225","DOIUrl":null,"url":null,"abstract":"<div><p>MiR-519e-5p and CTPS1 are aberrantly expressed in breast cancer (BC). However, the molecular mechanisms underlying tumorigenesis and development are unknown, and their potential as therapeutic targets needs to be explored. The molecular biology was explored through in vitro cellular experiments, tumor xenograft assay, and analysis of gene expression in human tissue and serum samples. We found that miR-519e-5p expression was much lower and CTPS1 expression was much higher in BC tissues and cells than in the normal tissues and cells. BC cells overexpressing miR-519e-5p or CTPS1 knockdown demonstrated decreased proliferation, migration, and invasion, whereas miR-519e-5p knockdown had the opposite effect. Further studies showed that there is a binding site between miR-519e-5p and CTPS1, leading to their interaction, CTPS1 overexpression and could partially reverse the inhibitory effects of miR-519e-5p overexpression on cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). CTPS1 serum levels were higher in patients with BC, and these levels were associated with some highly correlated clinical indicators, including age, HER-2 index, and T and N staging. Overall, miR-519e-5p slows the proliferation, invasion, migration, and EMT of BC by binding to CTPS1. This study offers a new direction for BC treatment.</p></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":null,"pages":null},"PeriodicalIF":3.3000,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental cell research","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0014482724003161","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
MiR-519e-5p and CTPS1 are aberrantly expressed in breast cancer (BC). However, the molecular mechanisms underlying tumorigenesis and development are unknown, and their potential as therapeutic targets needs to be explored. The molecular biology was explored through in vitro cellular experiments, tumor xenograft assay, and analysis of gene expression in human tissue and serum samples. We found that miR-519e-5p expression was much lower and CTPS1 expression was much higher in BC tissues and cells than in the normal tissues and cells. BC cells overexpressing miR-519e-5p or CTPS1 knockdown demonstrated decreased proliferation, migration, and invasion, whereas miR-519e-5p knockdown had the opposite effect. Further studies showed that there is a binding site between miR-519e-5p and CTPS1, leading to their interaction, CTPS1 overexpression and could partially reverse the inhibitory effects of miR-519e-5p overexpression on cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). CTPS1 serum levels were higher in patients with BC, and these levels were associated with some highly correlated clinical indicators, including age, HER-2 index, and T and N staging. Overall, miR-519e-5p slows the proliferation, invasion, migration, and EMT of BC by binding to CTPS1. This study offers a new direction for BC treatment.
期刊介绍:
Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.