Knockdown of long non‑coding RNA HCP5 suppresses the malignant behavior of retinoblastoma by sponging miR‑3619‑5p to target HDAC9.

Abstract

A number of studies have verified the vital effects of long non‑coding RNAs on the malignant behaviour of retinoblastoma (RB). The objective of the present study was to examine the specific role and mechanisms of HLA complex P5 (HCP5) in RB. For this purpose, reverse transcription‑quantitative polymerase chain reaction was used to determine the expression of HCP5, microRNA (miRNA/miR)‑3619‑5p and histone deacetylase 9 (HDAC9). A 3‑(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2‑H-tetrazolium bromide assay was conducted to detect cell viability. Transwell assays were used to evaluate the abilities of cell migration and invasion. A mouse tumor model was established to explore the functions of HCP5 in RB invivo. The interactions between HCP5, miR‑3619‑5p and HDAC9 were confirmed by a dual‑luciferase reporter assay. The protein expression of HDAC9 was determined by western blot analysis. The results revealed that the expression levels of HCP5 and HDAC9 were upregulated, whereas those of miR‑3619‑5p were downregulated in RB tissues and cell lines. The downregulation of HCP5 or the overexpression of miR‑3619‑5p suppressed RB cell proliferation, migration and invasion invitro. Simultaneously, the knockdown of HCP5 suppressed tumor growth in mice invivo. In addition, HCP5 was directly bound to miR‑3619‑5p and inversely correlated with miR‑3619‑5p. HDAC9 was found to be a target gene of and negatively regulated by miR‑3619‑5p. HCP5 expression also positively correlated with HDAC9 expression. Rescue experiments revealed that the overexpression of HDAC9 or the inhibition of miR‑3619‑5p reversed the inhibition of RB cell viability, migration and invasion induced by the knockdown of HCP5. On the whole, the present study demonstrates that the silencing of HCP5 exerts an anti‑tumor effect in RB by sponging miR‑3619‑5p to target HDAC9.