Abstract
BackgroundLung adenocarcinoma (LAD) is one of the most frequently diagnosed pathological categories of human lung cancer. Nevertheless, the link between long non-coding RNA (lncRNA) LINC01116 and LAD remains poorly investigated.MethodsQRT-PCR and western blot were applied for quantifying the expression of RNAs and proteins. Both functional experiments assays in vitro and xenografts model in vivo were implemented for analyzing LINC01116 function in LAD while molecular relationship among RNAs was investigated via mechanism experiments.ResultsLINC01116 was expressed at an abnormally high level in LAD, which was induced by transcription activator EGR1. LINC01116 depletion restrained proliferation, migration and invasion, yet facilitated apoptosis of LAD cells. MiR-744-5p could bind to LINC01116. MiR-744-5p inhibitor reversed the inhibitory effects of silencing LINC01116 on LAD malignant behaviors. In addition, cell division cycle-associated protein 4 (CDCA4) shared binding sites with miR-744-5p. Silencing LINC01116 elicited decline in CDCA4 mRNA and protein levels. Moreover, CDCA4 up-regulation could counteract the biological effects of LINC01116 knockdown on LAD cells.ConclusionOur data revealed that LINC01116 promoted malignant behaviors of LAD cells by targeting miR-744-5p/CDCA4 axis, implying the theoretical potential of LINC01116 as a novel target for LAD treatment.
Highlights
Lung adenocarcinoma (LAD) is one of the most frequently diagnosed pathological categories of human lung cancer
LINC01116 is markedly elevated in LAD cells and silencing LINC01116 can restrain the carcinogenic behaviors of LAD cells To analyze the potential role of LINC01116 in LAD, qRT-PCR analysis was implemented to detect the expression of LINC01116 in LAD cells
It manifested that LINC01116 was markedly elevated in LAD cells compared with HBE cells (Fig. 1A)
Summary
Lung adenocarcinoma (LAD) is one of the most frequently diagnosed pathological categories of human lung cancer. The link between long non-coding RNA (lncRNA) LINC01116 and LAD remains poorly investigated. The close association between the abnormal expression level of lncRNA and tumor cell growth and migration has been fathomed out in the past publications [8, 9]. It has been suggested in accumulating literatures that lncRNAs could exert specific functions, with competing endogenous RNAs (ceRNAs) network involved, by serving as miRNA sponges in post-transcriptional mediation [10]. It has been proved that LINC01116 could promote gefitinib resistance in nonsmall cell lung cancer via modulation of IFI44 [12]. Its performance and potential mechanism in LAD remain unclear
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