| Summary: | Background: Even though the role of long non-coding RNA H19 (lncRNA-H19) in diverse cancer types has been studied, exact effect of lncRNA-H19 as well as the underlying mechanism in retinoblastoma (RB) is poorly reported. We aimed to explore the possible functions of lncRNA-H19 in human RB Y79 cells. Methods: LncRNA-H19 in Y79 cells was silenced, and effects of lncRNA-H19 silence on cell viability, migration and invasion, and apoptosis were analyzed by using trypan blue exclusion, Transwell assay, and flow cytometry assay/Western blot analysis, respectively. Then, miR-143 expression in cells with lncRNA-H19 silence was determined by RT-qPCR, and effects of miR-143 inhibition on lncRNA-H19-suppressing cells were assessed. Whether RUNX2 was a target of miR-143 and the involved signaling pathways in the modulation of miR-143 were also studied. Results: LncRNA-H19 knockdown repressed cell viability, migration and invasion while promoted apoptosis in Y79 cells. miR-143 was a downstream factor of lncRNA-H19, and its inhibition reversed the effects of lncRNA-H19 silence on Y79 cells. RUNX2 was a target gene of miR-143, and miR-143 was found to affect Y79 cells via down-regulation of RUNX2. Phosphorylation of key kinases related in the PI3K/AKT/mTOR pathways was reduced by miR-143 via regulation of RUNX2. Conclusion: Knockdown of lncRNA-H19 acted a tumor suppressive role in Y79 cells through up-regulating miR-143. Moreover, miR-143 exerted tumor suppressive effects on Y79 cells by targeting RUNX2, along with inhibition of the PI3K/AKT/mTOR pathways.
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