MicroRNA-382 inhibits cell proliferation and invasion of retinoblastoma by targeting BDNF-mediated PI3K/AKT signalling pathway

It has previously been demonstrated that multiple microRNAs (miRNAs or miRs) are aberrantly expressed in retinoblastoma (RB) and contribute to RB initiation and progression. miR-382 has been revealed to be aberrantly expressed and therefore exhibits a key role in the progression of various types of cancer. However, the expression pattern, functional roles and underlying molecular mechanism of miR-382 in RB remain unknown. The present study investigated the expression levels of miR-382 and its effects on RB cells and the underlying regulatory mechanism of its action. It was demonstrated that miR-382 was downregulated in RB tissues and cell lines. Upregulation of miR-382 inhibited RB cell proliferation and invasion in vitro. Additionally, brain-derived neurotrophic factor (BDNF) was identified as a novel target of miR-382 in RB. BDNF was upregulated in RB tissues and negatively associated with miR-382 expression levels. Furthermore, BDNF overexpression rescued the tumour-suppressing effects on RB cells induced by miR-382. miR-382 inactivated the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signalling pathway in RB. These findings suggested that miR-382 serves as a tumour suppressor in RB, in part, by targeting the BDNF-mediated PI3K/AKT signalling pathway. The results of the present study suggest a potential therapeutic strategy for treating RB patients in the future.