Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Aug 25;13:8475–8493. doi: 10.2147/OTT.S235022

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2020 Liu et al.

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).

PMC Copyright notice

GAST was the direct target gene of miR-30a-3p in GC. (A) Cluster analysis of miR-30a-3p expression patterns in our GC miRNA profiling data. (B) The binding sites of miR-30a-3p sequences in the CDS of GAST gene. (C) qPCR analysis detected miR-30a-3p expression levels in a panel of gastric cell lines. U6 was used as the endogenous control for microRNA expression analysis. (D) Histogram showing the expression of GAST and miR-30a-3p in GC tissues and matched normal tissues. The levels of GAST mRNA were quantified by RT-PCR analysis. TaqMan qPCR analysis of miR-30a-3p in 10 paired GC samples. (E) The apparently inverse correlation between GAST and miR-30a-3p expression in gastric cell lines. (F) RT-PCR (upper) and Western blots (lower) analyses were used to monitor the effect of miR-30a-3p on the expression level of GAST in BGC823 and N87 GC cells liens. (B) RT-PCR (upper) and Western blot (lower) analyses were used to monitor the effect of miR-30a-3p inhibitor or mimics on the expression level of GAST in GC cell lines, which indicated the potential inverse correlation between miR-30a-3p and GAST. (G) ISH and IHC staining assays were used to detect the expression patterns of miR-30a-3p and GAST in 31 cases of GC and matched normal ones, respectively. (A) MiR-30a-3p was highly expressed in normal tissues. (C, E) Decreased or absent miR-30a-3p expression was detected in GCs. (B) Decreased or absent GAST expression was detected in normal tissues. d, f. GAST was highly expressed in GCs. (G) DIG-labeled LNA snRNA U6 probe were used as the positive control. DIG-labeled LNA scrambled sequence probe was used as the negative control. There was a statistically significant inverse correlation between miR-30a-3p and GAST (R=−0.265, p<0.01) in these samples. (H) The results from three independent dual-luciferase reporter assays indicated that GAST was the direct targeting of miR-30a-3p. Compared with the mutant-type and wild-type of GAST CDS groups, the reporter assays showed a significantly decreased luciferase activity in the wild-type group. *p<0.01.