Purpose: This study aimed to explore the role of MIR31HG and its molecular mechanism in breast cancer (BC).
Methods: The levels of MIR31HG in BC tissues and cell lines were detected. The correlations of MIR31HG expression level with clinical characteristics and prognosis of patients were analyzed. Then we detected the effects of MIR31HG on the proliferative, migrative and invasive abilities of BC cells. Subsequently, we detected the level of the predicted target POLDIP2 in BC. Furthermore, the effect of POLDIP2 on the malignant phenotype of MIR31HG-mediated BC was evaluated through recovery experiments.
Results: MIR31HG was aberrantly up-regulated in BC tissues and cell lines, and its level was in correlation with the patient's tumor diameter, tumor node metastasis (TNM) stage, lymph node metastasis as well as the overall survival rate. Besides, MIR31HG knockdown was able to inhibit the proliferative ability, migration and invasion of BC cells. Besides, POLDIP2 was aberrantly up-regulated in BC tissues, and its expression level was in positive correlation with the level of MIR31HG. Besides, POLDIP2 overexpression could partially inhibit the proliferative, migrative and invasive abilities of BC cells. Long non-coding (lnc)RNA MIR31HG was aberrantly up-regulated in BC and its expression was associated with poor prognosis of BC patients. Additionally, the levels of MIR31HG and POLDIP2 were positively correlated.
Conclusions: The low expression of MIR31HG or POLDIP2 can inhibit the proliferative, migrative and invasive abilities of BC cells, which provides a new target for the diagnosis along with the treatment of BC.