miR‑143‑5p suppresses breast cancer progression by targeting the HIF‑1α‑related GLUT1 pathway

Abstract

Breast cancer (BC) is a commonly identified life‑threateningtypeofcancerandamajorcauseofdeathamong women worldwide. Several microRNAs (miRs), including miR‑143‑5p, have been reported to be vital for regulating hallmarks of cancer; however, the effect of miR‑143‑5p on BC requires further exploration. The present study performed bioinformatics analysis on GSE42072 and GSE41922 datasets from the National Center for Biotechnology Information Gene Expression Omnibus (GEO) database to identify miR‑143‑5p expression patterns. Furthermore, miR‑143‑5p expression was detected in BC cell lines and tissues via reverse transcription‑quantitative PCR. Post‑transfection with miR‑143‑5p mimics, Cell Counting Kit‑8, colony formation and Transwell assays were performed to explore the effects of miR‑143‑5p on BC cell proliferation, colony formation, and migration. The association of miR‑143‑5p with the hypoxia‑inducible factor‑1α (HIF‑1α)‑associated glucose transporter 1 (GLUT1) pathway was explored via western blot‑ ting, immunofluorescence and dual‑luciferase reporter assay. The present study detected high expression of miR‑143‑5p in BC tissue of the GSE42072 and serum of the GSE41922 datasets by GEO chip analysis. Additionally, the expression levels of miR‑143‑5p were decreased in BC tissues compared with those in adjacent healthy tissues, and low miR‑143‑5p expression was associated with a poorer prognosis and shorter survival time in patients with BC. In vitro, miR‑143‑5p expres‑ sion levels were decreased in BC cells, and transfection with miR‑143‑5p mimics suppressed BC cell proliferation, colony formation, migration. Furthermore, miR‑143‑5p targeted the HIF‑1α‑related GLUT1 pathway, and inhibited HIF‑1α and GLUT1 expression. Additionally, HIF‑1α agonists reversed the miR‑143‑5p‑induced inhibition during tumorigenesis. In conclusion, miR‑143‑5p exhibited low expression in BC tissues, and suppressed BC cell proliferation, colony forma‑ tion, migration. Moreover, the antitumor effects of miR‑143‑5p targeted the HIF‑1α‑related GLUT1 pathway.