Long non-coding RNA KCNQ1OT1 promotes proliferation, migration and invasion via targeting miR-134 in retinoblastoma.

Abstract

Long non-coding RNAs (lncRNAs) exert a significant role in carcinogenesis. lncRNA KCNQ1OT1 is detected in many tumors and is considered as an oncogene. The expression and mechanism of KCNQ1OT1 in retinoblastoma (Rb) are not clearly elucidated. KCNQ1OT1, miR-134 and TRIM44 mRNA expression were examined by a quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR). Proliferation, migration and invasion of Weri-Rb1 and Y79 cells were tested by cell counting kit-8, colony formation, scratch and transwell assays. Meanwhile, the regulatory relationships among KCNQ1OT1, miR-134 and TRIM44 were clarified by several biological experiments, including dual-luciferase reporter assay, RNA immunoprecipitation, subcellular distribution, qRT-PCR and western blotting. lncRNA KCNQ1OT1 was up-regulated in Rb tissues and Rb cell lines. In addition, the expression of KCNQ1OT1 was negatively correlated with the disease-free survival rate of RB patients. Silencing KCNQ1OT1 could significantly inhibit the RB progression in vivo and in vitro. The analysis of the mechanism of KCNQ1OT1 showed that KCNQ1OT1 can sponge miR-134, and miR-134 may inhibit TRIM44 expression. Moreover, the rescue assays showed that KCNQ1OT1 promoted RB progression by regulating the miR-134/TRIM44 pathway. The present study indicates that a new KCNQ1OT1/miR-134/TRIM44 pathway regulates Rb progression. It may be used as a potential prognostic marker for Rb.