LncRNA LET function as a tumor suppressor in breast cancer development.

Abstract

To evaluate the effect of long-chain non-coding RNA LET (lncRNA LET) on the regulatory of human breast cancer and its underlying mechanism. The expression levels of lncRNA LET in breast cancer tissues, MDA-MB-231 cells and MCF-10A breast epithelial cells were detected by quantitative Real-Time Polymerase Chain Reaction (qRT-PCR). The proliferation of lncRNA LET was detected by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide). Cell apoptosis was examined via flow cytometry. The invasion and migration of cells were detected by transwell and scratch assay. The expression of lncRNA LET was reduced in breast cancer tissues and MDA-MB-231 cells. Overexpression of lncRNA LET resulted in the inhibition of cell proliferation, invasion and migration ability, and promotion of cell apoptosis (p<0.05). Up-regulation of lncRNA LET repressed epithelial mesenchymal transition (EMT) process. LncRNA LET is a new type of molecule involved in the development of breast cancer, which may become a potential target for the treatment of breast cancer.