Regulatory effect of the MAFG?AS1/miR?150?5p/MYB axis on the proliferation and migration of breast cancer cells.

ABSTRACT: Long noncoding RNA (lncRNA) MAF BZIP transcription factor G antisense RNA 1 (MAFG?AS1) has been demonstrated to serve an important role in the progression of various types of cancer, whereas its role in breast cancer has not been fully elucidated. The present study aimed to explore the potential role and underlying mechanism of MAFG?AS1 in breast cancer. To achieve this, the expression of MAFG?AS1, microRNA (miR)?150?5p and MYB was detected by reverse transcription?quantitative PCR. The binding between miR?150?5p and MAFG?AS1 or MYB was verified using a luciferase reporter assay. Cell proliferation was analyzed by MTS, apoptosis and cell cycle were detected by Annexin V/propidium iodide, and cell migration was analyzed by wound healing assay. The results demonstrated that the expression levels of MAFG?AS1 were significantly upregulated in breast cancer tissues and cells compared with those in normal breast tissues and cells. High MAFG?AS1 expression promoted the proliferation, migration and epithelial?mesenchymal transition of breast cancer cells. By contrast, miR?150?5p expression was reduced in breast cancer tissues compared with that in healthy breast tissues, and low expression of miR?150?5p was associated with poor overall survival in patients with breast cancer. Bioinformatics and luciferase assay revealed that MAFG?AS1 served as a sponge of miR?150?5p, and that miR?150?5p bound to MYB. The functional rescue assay results demonstrated that MAFG?AS1 knockdown suppressed the proliferation and migration of breast cancer cells by regulating miR?150?5p, which in turn targeted MYB. In conclusion, the results of the present study demonstrated that MAFG?AS1 functioned as a novel oncogenic lncRNA in the development of human breast cancer via regulating the miR?150?5p/MYB axis, which suggested that MAFG?AS1 may be a novel biomarker for the diagnosis and prognosis of human breast cancer.

SUBMITTER: Jia H 

PROVIDER: S-EPMC7721084 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature