Long non‑coding RNA SNHG14 affects the proliferation and apoptosis of childhood acute myeloid leukaemiacells by modulating the miR‑193b‑3p/MCL1 axis.

Abstract

The purpose of the present study was to determine the biological function and associated regulatory mechanism of small nucleolar RNA host gene14 (SNHG14) in childhood acute myeloid leukaemia(AML). SNHG14 expression was measured via RT‑qPCR in bone marrow tissues from 57patients with AML and 57 healthy donors. The clinicopathological features of AML patients with low and high SNHG14 expression were analysed. AML cell viability and apoptosis were assessed using MTT and flow cytometry analyses. The starBase online database, and RNA‑binding protein immunoprecipitation and dual luciferase reporter gene assays were employed to analyse the interactions among SNHG14, microRNA(miR)‑193b‑3p and MCL1 apoptosis regulator BCL2 family member(MCL1). SNHG14 was found to be overexpressed in the bone marrow tissues of patients with AML. The French‑American‑British classification and cytogenetics were significantly different between patients with high and low expression of SNHG14. Silencing SNHG14 decreased AML cell proliferation and facilitated apoptosis. SNHG14 functioned as a sponge for miR‑193b‑3p, and miR‑193b‑3p decreased the viability and accelerated the apoptosis rate of AML cells. In addition, miR‑193b‑3p targeted MCL1. Furthermore, silencing SNHG14 resulted in the sponging of miR‑193b‑3p to regulate cell viability, apoptosis, and MCL1 expression in AML. SNHG14 silencing decreased the viability and promoted apoptosis of AML cells by modulating the miR‑193b‑3p/MCL1 axis.