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, miRâ613 and câmet to viability, apoptosis and proliferation of retinoblastoma cells. Totally 276 retinoblastoma tissues and tumourâadjacent tissues were collected, and human retinoblastoma cell lines (ie, Y79, HXOâRb44, SOâRb50 and WERIâRB1) were also gathered. Moreover, transfections of pcDNA3.1âHOTAIR, siâHOTAIR, miRâ613 mimic, miRâ613 inhibitor, pcDNA3.1/câmet were performed to evaluate the influence of HOTAIR, miRâ613 and câmet on viability, apoptosis and epithelialâmesenchymal transition (EMT) of retinoblastoma cells. Dualâluciferase reporter gene assay was also arranged to confirm the targeted relationship between HOTAIR and miRâ613, as well as between miRâ613 and câmet. Consequently, upâregulated HOTAIR and downâregulated miRâ613 expressions displayed associations with poor survival status of retinoblastoma patients (P < 0.05). Besides, inhibited HOTAIR and promoted miRâ613 elevated Eâcadherin expression, yet decreased Snail and Vimentin expressions (P < 0.05). Simultaneously, cell proliferation and cell viability were also lessâmotivated (P < 0.05). Nonetheless, câmet prohibited the functioning of miRâ613, resulting in promoted cell proliferation and viability, along with inhibited cell apoptosis (P < 0.05). Finally, HOTAIR was verified to directly target miRâ613, and câmet was the direct target gene of miRâ613 (P < 0.05). In conclusion, the role of lncRNA HOTAIR/miRâ613/câmet signalling axis in modulating retinoblastoma cellsâ viability, apoptosis and expressions of EMTâspecific proteins might provide evidences for developing appropriate diagnostic and treatment strategies for retinoblastoma.