Lung adenocarcinoma (LUAD) is the most common lung cancer with high incidence. The prognosis of LUAD is poor due to its aggressive behavior. Long non‑coding RNAs (lncRNAs) have been reported as a key modulator on LUAD progression. Therefore, the present study aimed to clarify the molecular mechanism of lncRNAs in LUAD development. The expression of lncRNA RP11‑805J14.5 (RP11‑805J14.5) in LUAD tissues and cells was quantified based on the data in The Cancer Genome Atlas (TCGA). Cell viability was determined using Cell Counting Kit‑8 method. Apoptotic cells were sorted and determined by flow cytometry. Cell migration and invasion abilities were detected by the Transwell assay. Luciferase reporter experiment and RNA pull‑down assay were utilized to determine the interactions between RP11‑805J14.5, microRNA (miR)‑34b‑3p, miR‑139‑5p, and cyclin D2 (CCND2). A xenograft tumor was established to determine tumor growth in vivo. RP11‑805J14.5 was highly expressed in LUAD and associated with poor survival of LUAD patients. Knockdown of RP11‑805J14.5 suppressed LUAD cell growth, invasion, migration and tumor growth, indicating that RP11‑805J14.5 is an important regulator of LUAD. Our study demonstrated that the regulation of RP11‑805J14.5 on LUAD was mediated by CCND2 whose expression was regulated by sponging miR‑34b‑3p and miR‑139‑5p. The expression of RP11‑805J14.5 was increased in LUAD, and the knockdown of RP11‑805J14.5 expression suppressed LUAD cell growth, invasion and migration by downregulating CCND2 by sponging miR‑34b‑3p and miR‑139‑5p, indicating that RP11‑805J14.5 could be a prospective target for LUAD therapy.
Keywords: RP11‑805J14.5; cyclin D2; lung adenocarcinoma; microRNA‑139‑5p; microRNA‑34b‑3p.