Abstract
This study aimed to explore the role and potential mechanism of the long non-coding (lncRNA) MBNL1-AS1 in human breast cancer. We included 80 patients with breast cancer in this study. Breast cancer cell lines, including MCF7, SKBR3, MDA-MB-231 and MDA-MB-415, and the normal human breast cell line MCF10A were used in this study. MBNL1-AS1, miR-889-3p mimics, si-Krüppel-like factor 9 (KLF9) or their controls were transfected in the cells. Quantitative reverse transcription polymerase chain reaction (qRT-PCR), Western blotting and immunohistochemistry assay were performed to detect the expression of MBNL1-AS1, miR-889-3p and KLF9. Cell proliferation, invasion and migration were detected. Luciferase reporter gene and pull-down assay were performed to verify the target relationship among MBNL1-AS1, miR-889-3p and KLF9. Glycolysis was also detected after transfection. The expression of the lncRNA MBNL1-AS1 was low in the breast cancer tissues and cells. Lower expression levels of the lncRNA MBNL1-AS1 were associated with poor prognosis of breast cancer. Overexpression of the lncRNA MBNL1-AS1 decreased proliferation, invasion, migration and glycolysis of breast cancer cells. The lncRNA MBNL1-AS1 could interact with miR-889-3p, and KLF9 was the downstream target of miR-889-3p. Moreover, miR-889-3p was negatively correlated with KLF9 and lncRNA MBNL1-AS1. Both miR-889-3p and si-KLF9 could reverse the overexpression of lncRNA MBNL1-AS1 in breast cancer development. The lncRNA MBNL1-AS1 decreased proliferation, invasion, migration and glycolysis of breast cancer via the miR-889-3p/KLF9 axis, which might be a potential biomarker for the diagnosis of breast cancer.