MicroRNA-655 attenuates the malignant biological behaviours of retinoblastoma cells by directly targeting PAX6 and suppressing the ERK and p38 MAPK signalling pathways.

Numerous studies have indicated that microRNAs (miRNAs) regulate signalling molecules by acting as oncogenes or tumour-suppressor genes in retinoblastoma (RB). Therefore, investigation of the expression pattern, biological roles and associated mechanisms of cancer-related miRNAs in RB may provide novel therapeutic targets for patients with this disease. miRNA-655 (miR-655) has been reported to be aberrantly expressed in many types of cancers. However, the expression pattern, detailed biological function and underlying molecular mechanisms of miR-655 in RB remain to be clarified. Therefore, the aims of the present study were to detect miR-655 in RB, investigate its biological roles in RB and determine the underlying molecular mechanisms. The results of the present study showed that miR-655 was significantly downregulated in RB tissues and cell lines. Overexpression of miR-655 inhibited the proliferation and invasion ability while it increased the apoptosis of RB cells. Additionally, paired box 6 (PAX6) was identified as a direct target of miR-655 in RB. Furthermore, PAX6 was highly expressed in RB tissues and was negatively correlated with miR-655 expression. PAX6 knockdown recapitulated effects similar to those observed following miR-655 overexpression regarding the proliferation, invasion and apoptosis of RB cells. Rescue experiments demonstrated that restoration of PAX6 expression reversed the tumour-suppressing roles of miR-655 in RB cells. Moreover, upregulation of miR-655 reduced activation of the extracellular signal-regulated kinase and p38 mitogen-activated protein kinase signalling pathways in RB cells through PAX6 regulation. Therefore, restoration of miR-655 expression may be a promising therapeutic strategy for treating patients with RB in the future.