LncRNA FOXD3-AS1 enhances the migration and invasion ability of breast cancer cells through the Wnt/β-Catenin signaling pathway

Objective: To explore the expression, biological function, and mechanism of action of the LncRNA FOXD3-AS1 in breast cancer. Methods The expression of LncRNA FOXD3-AS1 was analyzed in the TCGA database using bioinformatics analysis. Moreover, the relative expression of LncRNA FOXD3-AS1 was measured in the human normal mammary epithelial cell line (MCF10A) and three breast cancer cell lines (BT-549, MDA-MB-231, and MCF-7). After siRNA knockdown of FOXD3-AS1 expression in BT-549, MDA-MB-231 cells, alterations in cell proliferation, migration, invasion, and apoptotic capacity were determined by CCK-8, scratch assay, transwell assay, and Annexin V-FITC/PI staining, respectively. Furthermore, changes in the level of the β-Catenin protein were detected using western blot. Results TCGA database analysis results relative to adjacent tissues revealed that the expression of LncRNA FOXD3-AS1 was markedly elevated in breast cancer tissues. Besides, results of real-time PCR established that the relative expression of FOXD3-AS1 was significantly higher in the breast cancer cell lines (BT-549, MDA-MB-231, and MCF-7) than in the normal human mammary epithelial cell line (MCF10A) (P < 0.0001). Inhibition of FOXD3-AS1 expression by siRNA significantly inhibited the wound healing ability, migration and invasion ability of BT-549 and MDA-MB-231 cells. However, there was no difference in proliferation and apoptosis. The western blot results showed that inhibition of FOXD3-AS1 expression by siRNA significantly inhibited the level of the β-Catenin protein in BT-549 and MDA-MB-231 cells. Conclusion The abnormally high expression of LncRNA FOXD3-AS1 in breast cancer may be related to disease progression. LncRNA FOXD3-AS1 can significantly enhance the migration and invasion ability of breast cancer cells, and its mechanism of action may be related to the Wnt/ β-Catenin signaling pathway.