Linc-OIP5 loss regulates migration and invasion in MDA-MB-231 breast cancer cells by inhibiting YAP1/JAG1 signaling.

Breast cancer is the most prevalent cancer among women, and diagnosis and treatment represent a substantial challenge due to the lack of adequate molecular targets. It has been shown that long noncoding RNAs (lncRNAs) serve pivotal roles in regulating gene expression in tumors. The roles of long intervening noncoding RNA (Linc)-OIP5 has been demonstrated in different types of cancer; however, its function in breast cancer has not been determined. In the present study, expression of Linc-OIP5, YAP1 (Hippo signaling component) and JAG1 (Notch signaling component) in breast cancer cells with different degrees of malignancy were determined. To assess whether Linc-OIP5 regulated the malignant biological behaviors of MDA-MB-231 cells, its expression was knocked down using a specific small interfering RNA (siRNA), and cell proliferation was determined using a CCK-8 assay, apoptosis was evaluated using an Annexin V-FITC apoptosis detection kit, migration was assessed using a wound healing and transwell migration assays, and cell invasion examined using a transwell invasion assays. The effect of Linc-OIP5 knockdown on YAP1 and JAG1 expression was quantified using reverse transcription-quantitative PCR and immunoblotting. Cell proliferation, migration and invasion were reduced, while apoptosis was increased in MDA-MB-231 cells transfected with Linc-OIP5-specific siRNA. Mechanistic investigations showed that Linc-OIP5 knockdown downregulated YAP1 and JAG1 expression. The results of the present study suggest that Linc-OIP5 affects the malignant biological behaviors of MDA-MB-231 cells, at least partly through its effects on YAP1/JAG1 signaling. Whilst there are a number of mechanisms underlying the pathogenesis of breast cancer, the results of the present study highlight Linc-OIP5 as a potential therapeutic target in breast cancer. [ABSTRACT FROM AUTHOR]