Since lncRNAs could modulate neoplastic development by modulating downstream miRNAs and genes, this study was carried out to figure out the synthetic contribution of HOTAIR, miR-613 and c-met to viability, apoptosis and proliferation of retinoblastoma cells. Totally 276 retinoblastoma tissues and tumour-adjacent tissues were collected, and human retinoblastoma cell lines (ie, Y79, HXO-Rb44, SO-Rb50 and WERI-RB1) were also gathered. Moreover, transfections of pcDNA3.1-HOTAIR, si-HOTAIR, miR-613 mimic, miR-613 inhibitor, pcDNA3.1/c-met were performed to evaluate the influence of HOTAIR, miR-613 and c-met on viability, apoptosis and epithelial-mesenchymal transition (EMT) of retinoblastoma cells. Dual-luciferase reporter gene assay was also arranged to confirm the targeted relationship between HOTAIR and miR-613, as well as between miR-613 and c-met. Consequently, up-regulated HOTAIR and down-regulated miR-613 expressions displayed associations with poor survival status of retinoblastoma patients (P < 0.05). Besides, inhibited HOTAIR and promoted miR-613 elevated E-cadherin expression, yet decreased Snail and Vimentin expressions (P < 0.05). Simultaneously, cell proliferation and cell viability were also less-motivated (P < 0.05). Nonetheless, c-met prohibited the functioning of miR-613, resulting in promoted cell proliferation and viability, along with inhibited cell apoptosis (P < 0.05). Finally, HOTAIR was verified to directly target miR-613, and c-met was the direct target gene of miR-613 (P < 0.05). In conclusion, the role of lncRNA HOTAIR/miR-613/c-met signalling axis in modulating retinoblastoma cells' viability, apoptosis and expressions of EMT-specific proteins might provide evidences for developing appropriate diagnostic and treatment strategies for retinoblastoma.
Keywords: c-met; epithelial-mesenchymal transition; lncRNA HOTAIR; miR-613; retinoblastoma.
© 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.