Chromosome 8q24 lies in a gene desert with only a few predicted coding genes, but its variation is associated with multiple tumors. FAM83A in this region activates both PI3K/AKT/TOR and RAS/MAPK signaling cascades downstream of EGFR. The contribution of long noncoding gene in the antisense chain of FAM83A (RP11-539E17.5 and FAM83A-AS1) to the risk of lung adenocarcinoma (LUAD) need to be studied. We use systematic informatics method to identify the differential expression genes of the Cancer Genome Atlas (TCGA) LUAD transcriptome sequencing data. Then use data mining method to analysis the lncATLAS, USCS, Cistrome, and ENCODE database to infer the biological role of these two lncRNAs. Significant analysis of gene ontology (GO) terms enrichment analyzed the co-expression genes of RP11-539E17.5 in the LUAD and adjacent tissues. At last we use cell experiment to verify the lncRNA function. FAM83A-AS1 and RP11-539E17.5 located in Chromosome 8q24 were significantly different expressed between cancer and adjacent tissues (log2foldchange>5, p<0.05). The two lncRNA expression levels had notable correlation with FAM83A expression (coR> 0.8, P<0.005) and were significantly associated with patient overall survival and clinical stage (p<0.05). RP11-539E17.5, located in the enhancer element GH08J123181,belong to the enhancer lncRNA group. lncRNA subcellular localization data (lncATLAS) results showed that RP11-539E17.5 transcripts in K562 cells is mainly distributed in the nucleus, and most around the nucleolus and chromosomes. USCS, Cistrome, and ENCODE data mining identified four transcription factors (FOSL2, CTBP2, CEBPB, and MAFK) have significant correlation with the expression of FAM83A-AS1 and RP11-539E17.5. In K562 cell line with high expression of FAM83A-AS1, RP11-539E17.5 and FAM83A showed that expanded regions of RP11-539E17.5 gene sequence were marked by enhancer-specific modifications (H3K27ac domains and H3K4me3 domains). This region also showed an excellent source of DNase sensitive site, and with several binding sites for CTCF, FOSL2, CTBP2, CEBPB and MAFK. In addition, RP11-539E17.5 gene also with enriched DNA methylation feature. RP11-539E17.5 and FAM83A-AS1 knocked down both inhibited the expression of FAM83A the proliferation of PC9, and RP11-539E17.5 gene owning a more significant effect. GO terms enrichment analysis of the co-expressed genes with RP11-539E17.5 showed that the most significantly activated biological pathways is involved with Cell cycle,and cell mitotic signaling pathway, while the molecular function involved with transcription factor binding, DNA binding, ATP binding, endonuclease activity, DNA topoisomerase activity. We found a LncRNA RP11-539E17.5 with enhancer character up regulate FAM83A expression in LUAD. These results can lay a theoretical foundation for LUAD corresponding countermeasures.