LncRNA LOXL1-AS1 inhibited cell proliferation, migration and invasion as well as induced apoptosis in breast cancer via regulating miR-143-3p

摘要

OBJECTIVE: In recent years, studies have shown that lncRNA plays an essential regulatory role in biological life activities. In disease and cancer research, the function of lncRNA is closely related to inflammatory response, tumor formation and cellular metabolism. Breast cancer is one of the most common malignant tumors in women. The research on the pathogenesis of breast cancer is the focus of current research. Although the regulatory mechanisms of some lncRNAs have been proven, the complexity of cancer regulation has led to incomplete research. MATERIALS AND METHODS: The expression of LOXL1-AS1 and miR-143-3p was measured using qRT-PCR. Western blot was used to detect CDK, Cyclin D1, MMP-2, MMP-9, Bcl-2, Bax and Cleaved caspase-3 protein expression. MTT assay and transwell assay were applied to analyze cell proliferation, migration and invasion, respectively. Cell apoptosis rate of transfected cells was measured with flow cytometry. Luciferase reporter assay was applied to verify the relationship between LOXL1-AS1 and miR-143-3p. RESULTS: In this study, we found that LOXL1-AS1 expression was induced while miR-142-3p expression was decreased in breast cancer tissues and cells, implying that LOXL1-AS1 and miR-143-3p play an important role in cell progression of breast cancer. Further investigation showed that silencing LOXL1-AS1 inhibited proliferation, promoted cell apoptosis and decreased the capacity of cell migrated and invasive in breast cancer cells. The analysis of luciferase reporter assay determined that LOXL1-AS1 directly targeted miR-143-3p in breast cancer cells. The rescue experiments further proved that miR-143-3p reversed the inhibited effects of si- LOXL1-AS1 on breast cancer cells. CONCLUSIONS: In this study, we verified that LncRNA LOXL1-AS1 inhibited cell proliferation, migration and invasion as well as induced apoptosis in breast cancer via regulating miR-143-3p, providing a novel therapeutic target and improving understanding of the regulatory mechanism of cell progression in breast cancer.