Inhibition of miR-660-5p expression suppresses tumor development and metastasis in human breast cancer.

Abstract

Breast cancer, which derives from the epithelium of the mammary glands, is one of the most common cancers diagnosed in women globally. To date, the authors of many studies have reported that the deregulation of microRNAs (miRNAs) plays a crucial role in the occurrence, development, and metastasis of tumors. Here, we discovered that miR-660-5p was upregulated in the breast cancer cell lines MCF7 and MDA-MB-231 compared with that in the normal control cell line CCD-1095Sk. We then inhibited the expression of miR-660-5p to investigate its biological function in cancer development, progression, and metastasis. We determined the changes in the levels of expression of transcription factor CP2 (TFCP2) and CDKN1A to further clarify the specific mechanism involved. The results showed that downregulation of miR-660-5p significantly suppressed the proliferation, migration, and invasion of MCF7 breast cancer cell. Moreover, inhibition of miR-660-5p promoted cell cycle G1 arrest and reduced apoptosis in breast cancer cells. The specific mechanism studies confirmed that TFCP2 was a direct downstream target of miR-660-5p. Aberrant expression of miR-660-5p repressed TFCP2 expression, whereas inhibition of miR-660-5p decreased TFCP2 protein expression, which is a vital factor in the downstream signaling pathway. In conclusion, miR-660-5p can regulate the proliferation, migration, and invasion of human breast cancer cells, and is a novel potential therapeutic target for the clinical treatment of breast cancer.