Molecular mechanisms of long chain non-coding RNA CTBP1-AS in regulation of invasion and migration of breast cancer cells.

This study aimed to investigate the role of long-chain non-coding RNA CTBP1-AS in breast cancer progression and cell invasion as well as migration. Clinical data of breast cancer patients (N = 155) in our hospital was collected for further analysis. qRT-PCR was used to detect LncRNA CTBP1-AS expression levels in human normal breast epithelial cell (MCF-10A) and breast cancer cells (MCF-7, BT- 549, MDA-MB-231 and MDA-MB-435). LncRNA CTBP1-AS knock-down and overexpressed lentivirus vectors were constructed to transfect breast cancer cells. Colony formation assay was employed to detect cell proliferative abilities. Flow cytometry was performed to detect cell apoptosis ratio. Wound healing scratch assay was used to detect cell migration, and Transwell matrigel assay was used to detect cell invasion. Bioinformatics analysis was performed to predict the downstream targets of LncRNA CTBP1-AS, which were further validated by dual-luciferase reporter gene system. The results showed that LncRNA CTBP1-AS was aberrantly overexpressed in breast cancer tissues and breast cancer cells compared to the control group. Moreover, the expression levels of LncRNA CTBP1-AS were positively related with tumor size, histological grade and the expression levels of Ki-67 and Her2. Further analysis showed that LncRNA CTBP1-AS expression levels negatively correlated with patient survival time and clinical prognosis. Of note, overexpressed LncRNA CTBP1-AS promoted breast cancer cell proliferation and invasion as well as migration, and decreased cell apoptosis ratio. Bioinformatics analysis and dual-luciferase reporter gene system results validated that microRNA-940 was the downstream target of LncRNA CTBP1-AS. Interestingly, overexpressed microRNA-940 abrogated the effects of LncRNA CTBP1-AS on cell proliferation, apoptosis, and invasion. In conclusion, overexpressed LncRNA CTBP1- AS promoted breast cancer cell proliferation, invasion as well as migration, inhibited cell apoptosis and accelerated breast cancer development by sponging microRNA-940.