It has been announced in accumulative studies that non-coding (nc)RNAs are responsible for a varieties of biological behaviors during the progression of tumors. As two subgroups of ncRNAs family, micro (mi)RNAs can interact with long non-coding (lnc)RNAs, thereby forming ceRNA network. In this study, miR-448 was expressed higher in NSCLC tissues (P < 0.01) and NSCLC cell lines (P < 0.01). Moreover, low expression of miR-448 predicted poor prognosis for patients with NSCLC (P < 0.001). Functional assays revealed the anti-oncogenic function of miR-448 in NSCLC by inhibiting cell proliferation, invasion, migration and epithelial-mesenchymal transition (EMT). Mechanically, miR-448 was found to be negatively regulated by lncRNA PRNCR1 (prostate cancer non-coding RNA 1). Moreover, HEY2 (Hairy and enhancer of split-related with YRPW motif protein 2) was demonstrated to be the target mRNA of miR-448 in NSCLC cells. All mechanism experiments revealed that lncRNA PRNCR1 exerted ceRNA function in NSCLC by regulating miR-448 and HEY2. To validate the function of PRNCR1-miR-488-HEY2 network in NSCLC progression, rescue assays were conducted. Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448.