The effects of aberrant expression of LncRNA DGCR5/miR-873-5p/TUSC3 in lung cancer cell progression.

Lung cancer is the most common cause of cancer-related mortality worldwide, and nonsmall cell lung cancer (NSCLC) accounts for 80% of all pulmonary carcinomas. Recently, long noncoding RNAs (lncRNAs) have been paid attention for exploring treatment of various diseases. Upregulation of DiGeorge syndrome critical region gene 5 (DGCR5) predicts better lung squamous cell carcinoma prognosis; therefore, we explore the role of DGCR5 in lung cancer in our present study. Consecutive patients with LC were treated in our hospital between January 2015 and January 2016. qRT-PCR demonstrated that DGCR5 was significantly lower in neoplastic tissues than in non-neoplastic tissues. For in vitro experiments, cell growth, migration, and invasion were significantly lower in A549 cells transfected with pcDNA3.1-DGCR5 than pcDNA3.1, which were verified by 5-diphenyltetrazolium bromide (MTT) assay, scratch test, and transwell assay, respectively, with no significant induction on cell apoptosis that was demonstrated by flow cytometry (FCM) assay. Bioinformatics analysis predicted that 3' untranslated region (UTR) of tumor suppressor candidate 3 (TUSC3, 49-55 bp) and DGCR5 (801-807 bp) shared a common hsa-miR-873-5p binding site, and the direct interaction between DGCR5 and hsa-miR-873-5p or hsa-miR-873-5p and TUSC3 was verified by dual-luciferase reporter assay. qRT-PCR demonstrated that hsa-miR-873-5p was dramatically higher and TUSC3 was significantly lower in neoplastic tissues than in non-neoplastic tissues. DGCR5 decreased the protein level of TUSC3 by miR-873-5p which was demonstrated by Western blot and immunofluorescence. The role of DGCR5 in tumorigenesis in vivo was consistent with in vitro assays, Ki-67-positive cell number (exhibited by immunohistochemical staining), tumor size, and tumor weight of A549-DGCR5 group were significantly lower in comparison with A549-control group.