RP11‑284F21.9 promotes lung carcinoma proliferation and invasion via the regulation of miR‑627‑3p/CCAR1.

Abstract

Lung carcinoma is a prominent cause of mortality among patients with cancer. Previous studies have reported the vital role of long non-coding RNAs (lncRNAs) in the malignant progression of lung cancer. lncRNA RP11-284F21.9 was originally identified to be expressed in lung carcinoma, but its specific function remains unknown. Therefore, the present study aimed to elucidate the role of lncRNA RP11-284F21.9 in lung carcinoma progression. The expression of RP11-284F21.9 in lung cell lines and tissues was measured using reverse transcription-quantitative PCR. The endogenous expression of RP11-284F21.9 was silenced using RNA interference, and cell viabilities were measured with a Cell Counting Kit-8 assay. The invasion and apoptosis of cells were determined via Transwell assays and flow cytometry, respectively. The protein expression levels were measured by western blotting. An increased expression of RP11-284F21.9 was identified in both lung carcinoma tissues and cells. Knockdown of RP11-284F21.9 in lung carcinoma cells inhibited cell proliferation and invasion, but promoted cell apoptosis. The present study identified the existence of a direct interaction between RP11-284F21.9 and microRNA (miRNA/miR)-627-3p. Mechanistically, it was demonstrated that RP11-284F21.9 promoted the proliferation and invasiveness of lung carcinoma cells, in part, via the regulation of miR-627-3p. Furthermore, cell division cycle and apoptosis regulator 1 (CCAR1) was identified as a target gene of miR-627-3p. The in vivo tumor growth assay also demonstrated that the knockdown of RP11-284F21.9 suppressed tumor growth, upregulated miR-627-3p and downregulated CCAR1 in the xenograft model of nude mice. Thus, the present findings indicated the tumor promoting functions of RP11-284F21.9 in the progression of lung carcinoma, and provided a novel lncRNA/miRNA axis as a target for the management of lung cancer.