NDRG2 Regulates the Expression of Genes Involved in Epithelial Mesenchymal Transition of Prostate Cancer Cells

Mohammad Moradi Monfared, Marziyeh Alizadeh Zarei, Gholamreza Rafiei Dehbidi, Abbas Behzad Behbahani, Rita Arabsolghar, Mohammad Ali Takhshid


Background: Metastasis is the main cause of prostate cancer (PCa) death. The inhibitory effect of N-myc downstream-regulated gene 2 (NDRG2) on the invasiveness properties of PCa cells has been demonstrated previously. However, its underlying mechanisms have not yet been investigated. The present study aimed to investigate the effects of NDRG2 overexpression on the expression of genes involved in epithelial-mesenchymal transition (EMT) including E-cadherin (E-CAD), α- and β-catenins, Slug and Snail, transforming growth factor (TGF)-α and -β, and vascular endothelial growth factor (VEGF). Methods: In the present in vitro study, LNCaP cells were divided into three groups, namely NDRG2 group (transfected with PSES-pAdenoVator-PSA-NDRG2-IRES-GFP plasmid), mock group (transfected with mock plasmid), and control group (without transfection). The effect of NDRG2 overexpression on the migration and invasion of LNCaP cells were investigated using the transwell assay. Real-time PCR was used for the evaluation of gene expression. For the statistical analyses, one-way ANOVA, student t test or Mann-Whitney U test were applied using the SPSS software (version 15.0). P values <0.05 were considered statistically significant.
Results: The results demonstrated that the overexpression of NDRG2 reduced the invasion and migration of LNCaP cells compared to the control and mock groups (P<0.001). A decreased expression of TGF-β (P=0.002), VEGF (P=0.014), Slug (P=0.005), and Snail (P=0.012); and an increased expression of E-CAD (P=0.009) were observed following NDRG2 overexpression in LNCaP cells.
Conclusion: The results of the present study suggest that NDRG2 inhibits the invasiveness properties of LNCaP cells probably through changes in the expression of genes involved in EMT.

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pISSN: 0253-0716         eISSN: 1735-3688