Long non-coding RNA MALAT1 aggravates human retinoblastoma by sponging miR-20b-5p to upregulate STAT3

Abstract

ObjectiveRetinoblastoma (RB) is an uncommon childhood carcinoma of the developing retina. Long non-coding RNA (lncRNA) metastasis associated lung adenocarcinoma transcript 1 (MALAT1), microRNA-20b-5p (miR-20b-5p) and signal transducer and activator of transcription 3 (STAT3) was revealed to partake in RB. But their relationship was still to be investigated, so we intended to discuss the specific interaction of MALAT1, miR-20b-5p and STAT3 in RB. MethodsBy RNA isolation and quantitation, we measured the MALAT1 expression in RB tissues and cell lines. Then, to determine the influence of MALAT1 on RB cells, RB cells were transfected with siRNA-MALAT1 or pcDNA-MALAT1. The interplay among MALAT1, miR-20b-5p and STAT3 were evaluated through dual luciferase reporter gene assay and RNA pull-down after RB cells treated with siRNA/pcDNA-MALAT1 or/and miR-20b-5p mimic/inhibitor. The influence of their interaction on cells was evaluated by cell counting kit-8, EdU assay and flow cytometry. Finally, the involvement of MALAT1 in tumorigenesis was elucidated in vivo. ResultsBoth RB tissues and cells showed highly expressed MALAT1. When MALAT1 was downregulated, RB cell proliferation was hindered and apoptosis was accelerated. MALAT1 sponged miR-20b-5p and upregulated STAT3. Silencing MALAT1 or overexpressing miR-20b-5p inhibited proliferation and promoted apoptosis in RB cells. The tumor growth of nude mice treated with siRNA-MALAT1 was inhibited. ConclusionMALAT1 could increase proliferation and reduce apoptosis by sponging miR-20b-5p to upregulate STAT3 in RB cells. Therefore, MALAT1 might be a latent target in the RB treatment.