Long noncoding RNA promotes breast cancer progression by functioning as a molecular sponge for microRNA-625 and thereby upregulating HMGA1.

Extensive research has shown that is aberrantly expressed in human cancers, and that dysregulation of is implicated in the initiation and progression of human cancers. The expression and functions of in breast cancer are still unclear. Our aims were to measure the expression of in breast cancer, determine its effects on malignant behaviors of tumor cells, and uncover the molecular events underlying the actions of in breast cancer. Herein, was found to be overexpressed in breast cancer samples, and its overexpression was correlated with lymph node metastasis, TNM stage and differentiation grade. Patients with breast cancer harboring higher expression showed shorter overall survival than did the patients with lower expression. Functional experiments revealed that depletion of inhibited breast cancer cell proliferation, migration, and invasion and facilitated apoptosis and impaired tumor growth . Mechanism investigation revealed that can interact with microRNA-625 (miR-625). worked as a competitive endogenous RNA for miR-625 to weaken the suppressive effect of miR-625 on high mobility group AT-hook 1 (HMGA1) in breast cancer cells. Furthermore, miR-625 inhibition and HMGA1 restoration both abrogated the effects of silencing on breast cancer cells. Our findings indicate that the -miR-625-HMGA1 pathway plays an important role in the malignancy of breast cancer and . Hence, targeting this pathway may be a novel strategy against breast cancer.