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. 2018 May 14;11:2797–2804. doi: 10.2147/OTT.S165147

Figure 5.

Figure 5

LncRNA GAPLINC acted as a molecular sponge of miR-378 in GC cells. SNU-1 cells were transfected with control, miR-378 mimics, or miR-378 mimics + pCDNA-GAPLINC. (A) Cell proliferation was measured by CCK-8 assay at the indicated times in SNU-1 cells. Results are represented as the mean ± SD. n = 4, ANOVA, *P < 0.05. (B) Cells were stained with propidium iodide (with RNase A). Cell cycle assay was measured using flow cytometry. Results are represented by three independent experiments. (C) The data of cell cycle were analyzed using Modifit software. Results are represented as the mean ± SD. n = 3, ANOVA, *P < 0.05. (D) The protein level of MAPK1 was analyzed by Western blotting assay. Results are represented by three independent experiments. (E) Quantitative analysis of MAPK1 protein level. Results are represented as the mean ± SD. n = 3, ANOVA, *P < 0.05. (F) The proposed signaling pathway underlying GAPLINC regulation of MAPK1 by miR-378 in GC cells.

Abbreviations: lncRNA, long noncoding RNA; GC, gastric cancer.