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. 2019 Aug 1;11:7263–7277. doi: 10.2147/CMAR.S211856

Figure 5.

Figure 5

SNHG16 functions as a ceRNA and regulates NRP1 expression in gastric cancer by competitively binding miR-628. (A) The predicted two binding sites for miR-628 on SNHG16 as predicted by bioinformatics software. (B) Agomir-628 or agomir-NC was cotransfected with wt-SNHG16 or mut-SNHG16 into BGC-823 and SGC-7901 cells, and sequentially the luciferase activity was quantified. *P<0.05 vs agomir-NC. (C) Expression of SNHG16 in 54 pairs of gastric cancer tissue samples and matched adjacent normal tissue samples was examined via RT-qPCR. *P<0.05 vs normal tissues. (D) Spearman’s correlation analysis uncovered an inverse association between miR-628 and SNHG16 in gastric cancer tissue samples. R2=0.4296, P<0.0001. (E) The expression levels of SNHG16 in BGC-823 and SGC-7901 cells when they were treated with si-SNHG16 or si-NC were determined by RT-qPCR. *P<0.05 vs si-NC. (F, G) RT-qPCR and Western blot analysis were performed to assess miR-628 and NRP1 protein expression, respectively, in SNHG16-depleted BGC-823 and SGC-7901 cells. *P<0.05 vs si-NC.