LncRNA LET function as a tumor suppressor in breast cancer development

C.-X. Zhou, X. Wang, N. Yang, S.-K. Xue, W.-C. Li, P.-P. Xie

Department of Thyroid Breast Surgery, Liaocheng People’s Hospital, Liaocheng, China. deji94741@163.com

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• Oncology

OBJECTIVE: To evaluate the effect of long-chain non-coding RNA LET (lncRNA LET) on the regulatory of human breast cancer and its underlying mechanism.

PATIENTS AND METHODS: 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.

RESULTS: 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.

CONCLUSIONS: 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.

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