Abstract
BackgroundThe expression of the long noncoding RNA LINC00483 is upregulated in lung adenocarcinoma (LUAD). However, its role in the progression of LUAD and the underlying mechanisms remain elusive.MethodsThe expressions of LINC00483 and miR-204-3p were determined using quantitative real-time PCR. The correlation between the clinicopathological characteristics of LUAD patients and LINC00483 expression was analyzed using Pearson’s χ2 test. A549 and PC-9 cells were transfected with small interfering RNA (siRNA) that specially targeting LINC00483 to assess the impact of its knockdown. Cell proliferation was assessed using the Cell Counting Kit-8 and clone forming assays. Cell migration and cell invasion were evaluated using a transwell assay. The levels of Snail, E-cadherin, N-cadherin and ETS1 proteins were determined via western blotting. The interaction between LINC00483 and miR-204-3p was analyzed using dual-luciferase, fluorescence in situ hybridization and RNA immunoprecipitation.ResultsLINC00483 was upregulated in LUAD tissues and cell lines. Higher LINC00483 levels closely correlated to shorter survival times, advanced TNM stage, larger tumor size and positive lymph node metastasis. Cell proliferation, migration and invasion were suppressed after LINC00483 knockdown. LINC00483 mainly localized in the cytoplasm, where it acted as a sponge of miR-204-3p. ETS1 was validated as a downstream target of miR-204-3p and is thus regulated by LINC00483.ConclusionThis study demonstrated that LINC00483 facilitates the proliferation, migration and invasion of LUAD cells by acting as a sponge for miR-204-3p, which in turn regulates ETS1.
Highlights
Lung cancer accounts for about one-quarter of cancer mortality, owing to its high invasiveness and rapid metastasis [1, 2]
We determined the expression of LINC00483 in lung adenocarcinoma (LUAD) tissues and non-tumor tissues (n = 60 in each group), finding that it was upregulated in the tumor tissues (Fig. 1b)
We found that the expression level of LINC00483 in LUAD cell lines was significantly higher than that in the pulmonary epithelial cell line BEAS-2B
Summary
Lung cancer accounts for about one-quarter of cancer mortality, owing to its high invasiveness and rapid metastasis [1, 2]. Non-small cell lung cancers (NCSLCs) account for more than 80% of all lung cancer cases. More than a half of NCSLCs are lung adenocarcinoma (LUAD), known as pulmonary adenocarcinoma. The survival rate of LUAD patients remains unsatisfactory despite the developments made in early. Exploring the molecular mechanisms underlying LUAD progression is of great importance to improving patient survival rates. The class includes long noncoding RNAs (lncRNAs), which are transcripts larger than 200 bp [4]. Increasing evidence has shown that mutations and aberrant expression of lncRNAs play a crucial role in cancers including LUAD [5, 6]. The expression of the long noncoding RNA LINC00483 is upregulated in lung adenocarcinoma (LUAD). Its role in the progression of LUAD and the underlying mechanisms remain elusive
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