Abstract

Suppressor of Zeste 12 homolog (SUZ12) is known to regulate tumor phenotype through altering gene expression, with an important regulatory role in tumor genesis and development. SUZ12 has been widely investigated; however, no studies regarding the role of the SUZ12 gene in retinoblastoma (RB) have been conducted. In this study, SUZ12 small interfering (si)RNA was transfected into SO-RB50 human RB cells. The influence of SUZ siRNA on RB cell invasion was detected using a soft agar colony forming assay and a Transwell cabin model. The effect of the SUZ12 siRNA on the expression levels of the associated proteins, vascular endothelial growth factor (VEGF), matrix metalloproteinase (MMP)-9 and MMP-2, was detected by western blotting. The number of cell clones was found to be reduced by the siRNA in a dose-dependent manner, and the number of cells that had permeated through the filter membrane was reduced following transfection with the siRNA. SUZ12 inhibition resulted in a marked reduction in VEGF, MMP-2 and MMP-9 expression levels (0.26±0.04, 0.16±0.02 and 0.12±0.02, respectively) compared with the levels in the non-transfected group (0.80±0.10, 0.94±0.16 and 1.15±0.18, respectively) (P<0.01). In conclusion, SUZ12 siRNA inhibited cell invasion and the expression of VEGF, MMP-2 and MMP-9 in SO-RB50 retinoblastoma cells.

Highlights

  • Retinoblastoma (RB) is a rare malignant tumor in infants and young children that, if left untreated, has the potential to greatly endanger vision and life [1]

  • Suppressor of Zeste 12 homolog (SUZ12) is critical for tumor pathogenesis and development [7], and may be involved in the regulation of tumor stem cells [8]

  • The present study revealed that SUZ12‐specific siRNA suppressed SO‐RB50 cell colony formation in soft agar in a concentration‐dependent manner (Fig. 2), demonstrating that SUZ12 interference hindered SO‐RB50 cell invasion

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Summary

Introduction

Retinoblastoma (RB) is a rare malignant tumor in infants and young children that, if left untreated, has the potential to greatly endanger vision and life [1]. Numerous genes have been implicated in the genesis and development of RB [2]. Suppressor of Zeste 12 homolog (SUZ12), is an important component of polycomb group protein (PcG), and is essential in cell proliferation, cell cycle and embryonic development processes [3,4]. SUZ12 is known to regulate tumor phenotype through altering gene expression, with an important regulatory role in tumor genesis and development, and this has been widely investigated [5]. To the best of our knowledge, no studies have analyzed the role of SUZ12 in RB and the underlying mechanism of action. The present study aimed to define the impact of SUZ12 on RB cell invasive ability, along with the potential underlying regulatory mechanism, with the aid of an SUZ12 RNA interference technique in the SO‐RB50 RB cell strain

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