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

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.