Abstract
BackgroundThis study aimed to explore the role and underlying molecular mechanisms of long non-coding RNA (lncRNA) LINC00342 in gastric cancer (GC).MethodsThe expression of LINC00342 in GC tissues was evaluated by Quantitative reverse transcription polymerase chain reaction (qRT-PCR). Silencing of LINC00342 was conducted to investigate the effect of LINC00342 in vitro and in vivo. The underlying molecular mechanisms of LINC00342 were determined by dual luciferase reporter assay, Western blotting analysis and rescue experiments. Biological functions of LINC00342 were evaluated by cell counting kit-8 (CCK-8) assay, colony formation assay, wound healing assay and Transwell assays. In addition, a tumor model was used to verify the effect of LINC00342 in tumorigenesis in vivo.ResultsLINC00342 was significantly upregulated in GC tissues and cell lines. Silencing of LINC00342 efficiently inhibited proliferation, migration and invasion of AGS cells in vitro, and also suppressed the tumorigenesis of GC in vivo. Functional experiments showed that LINC00342 regulated the expression of canopy fibroblast growth factor signaling regulator 2 (CNPY2) by competitively sponging miR-545-5p. Rescue experiments showed that inhibition of miR-545-5p and overexpression of CNPY2 significantly reversed cell phenotypes caused by silencing of LINC00342.ConclusionLINC00342 plays a potential oncogenic role in GC by targeting the miR545-5p/CNPY2 axis, and might act as a novel therapeutic target for GC.
Highlights
This study aimed to explore the role and underlying molecular mechanisms of long non-coding RNA LINC00342 in gastric cancer (GC)
LINC00342 was significantly upregulated in GC tissues To explore the role of LINC00342 in GC, the expression of LINC00342 in GC tissues was evaluated by Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and the results showed that LIC00342 was significantly upregulated in GC tissues (n = 30) compared with that in matched adjacent tissues (n = 30) (p < 0.01, Fig. 1a)
The expression of LINC00342 in GC tissues and matched adjacent tissues was evaluated by In situ hybridization (ISH) assay and the results showed that LINC00342 was obviously upregulated in GC tissues compared with that in matched adjacent tissues (Fig. 1d)
Summary
This study aimed to explore the role and underlying molecular mechanisms of long non-coding RNA (lncRNA) LINC00342 in gastric cancer (GC). Gastric cancer (GC) is one of the most aggressive malignancies and leading to a significantly increasing mortality in the world [1]. Long non-coding RNAs (lncRNAs), a class of ncRNAs with more than 200 nucleotides in length [4], have shown extensive biological functions in the pathogenesis of human cancers [5, 6]. It has been reported that lncRNAs function as competitive endogenous RNAs (ceRNAs) and compete for microRNA (miRNAs) to upregulate the expression of their target genes at the post-transcriptional level [7, 8]. LINC00342 is a newly identified lncRNA and significantly upregulated in nonsmall cell lung cancer [9].
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