PRDX6 Overexpression Promotes Proliferation, Invasion, and Migration of A549 Cells in vitro and in vivo

Abstract

Hao Li,1,* Donghua Zhang,2,* Bo Li,3 Honghua Zhen,4 Wenping Chen,4 Qingjuan Men5 1Department of Blood Transfusion, Shandong Provincial Hospital Affiliated with Shandong First Medical University, Shandong, 271016, People’s Republic of China; 2Department of Oncology, Zhangqiu People’s Hospital Shandong Province, Shandong, 250200, People’s Republic of China; 3Department of Orthopaedics, Central Hospital of XinWen Mining Group Co., Ltd., Shandong, 271233, People’s Republic of China; 4Department of Cardiothoracic Surgery, Zhangqiu District People’s Hospital, Jinan City, Shandong Province, 250200, People’s Republic of China; 5Clinical Laboratory, People’s Hospital of Juxian, Shandong, 276500, People’s Republic of China*These authors contributed equally to this workCorrespondence: Qingjuan MenClinical Laboratory, People’s Hospital of Juxian, No. 151 Shennong Road, Ju County, Rizhao City, Shandong, 276500, People’s Republic of ChinaTel [phone]Email [email protected]: Peroxiredoxin-6 (PRDX6) is frequently found in various cancers. However, its expression and relevance to proliferation, invasion, and migration in human non-small-cell lung cancer (NSCLC) remain unclear. This study investigated the role and novel mechanism of PRDX6 in progression in an NSCLC cell line (A549).Methods: We analyzed the expression of PRDX6 in NSCLC and adjacent normal tissues and explored the proliferation, migration, and invasion of A549 cells using either a PRDX6 plasmid or PRDX6 small interfering RNA (siRNA). We also assessed the effects of PRDX6 on the epithelial–mesenchymal transition (EMT) and β-catenin-mediated transcription of target genes.Results: PRDX6 expression was markedly higher in NSCLC tissues than in adjacent tissues. Proliferation, invasion, and migration of A549 cells were promoted by overexpression of PRDX6 but inhibited by its silencing. PRDX6 overexpression inhibited the protein expression of both phosphorylated β-catenin and E-cadherin, as well as the expression of vimentin, TWIST, and downstream targets of β-catenin including c-MYC, TCF-4, and MMP14. Conversely, PRDX6 silencing markedly decreased the expression of c-MYC, TCF-4, and MMP14, and inhibited EMT in A549 cells. Overexpression of PRDX6 in vivo notably increased the volume and weight of tumors.Conclusion: PRDX6 overexpression promotes the proliferation, invasion, and migration of A549 cells in vitro and in vivo.Keywords: PRDX6, non-small-cell lung cancer, β-catenin, metastasis, epithelial–mesenchymal transition

Keywords

• prdx6
• non-small cell lung cancer
• β-catenin
• metastasis
• epithelial-mesenchymal transition