MicroRNAs (miRNAs) have been demonstrated to participate in a variety of human cancers by functioning as post-transcriptional regulators of oncogenes or antioncogenes including non-small cell lung cancer (NSCLC). The aim of the current study was to identify the role of miR-422a in NSCLC sulfatase 2 (SULF2) to further elucidate the mechanism of NSCLC. Initially， the expression of miR-422a and SULF2 was determined in NSCLC tissues and cells. The role of miR-422a in NSCLC was identified in relation with a miR-422a mimic or inhibitor， siRNA against SULF2 and TGF-β1. The regulatory effects of miR-422a were examined following detection of the related epithelial mesenchymal transition (EMT)-related genes， and ... More
MicroRNAs (miRNAs) have been demonstrated to participate in a variety of human cancers by functioning as post-transcriptional regulators of oncogenes or antioncogenes including non-small cell lung cancer (NSCLC). The aim of the current study was to identify the role of miR-422a in NSCLC sulfatase 2 (SULF2) to further elucidate the mechanism of NSCLC. Initially， the expression of miR-422a and SULF2 was determined in NSCLC tissues and cells. The role of miR-422a in NSCLC was identified in relation with a miR-422a mimic or inhibitor， siRNA against SULF2 and TGF-β1. The regulatory effects of miR-422a were examined following detection of the related epithelial mesenchymal transition (EMT)-related genes， and the apoptosis-related genes and evaluation of their cellular biological functions. The expression pattern of miR-422a， SULF2， and the TGF-β/SMAD pathway-related genes was detected to elucidate the mechanism by which miR-422a influences the progression of NSCLC. Finally， xenograft tumors in nude mice were observed for tumorigenicity evaluation purposes. Our results showed that miR-422a was poorly expressed while SULF2 was highly expressed in NSCLC. Dual luciferase reporter gene assay further verified that miR-422a targeted SULF2. Altogether， this study demonstrated that miR-422a downregulated SULF2 to inhibit the TGF-β/SMAD pathway. NSCLC cell proliferation， migration， invasion， colony formation， EMT and tumorigenesis were all inhibited while apoptosis was promoted upon restoration of miR-422a or silencing of SULF2. However， the activation of the TGF-β/SMAD pathway was determined to reverse the tumor-suppressive effects of si-SULF2. miR-422a restoration， which ultimately inhibited the progression of NSCLC by suppressing the TGF-β/SMAD pathway SULF2.
