LAUSR

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.