Research Paper Volume 13, Issue 8 pp 12224—12238

Methylation of microRNA-338-5p by EED promotes METTL3-mediated translation of oncogene CDCP1 in gastric cancer

EED silencing upregulates miR-338-5p to restrain the proliferation and invasion of GC cells. (A) RT-qPCR to examine EED, miR-338-5p expression in response to si-EED and miR-338-5p inhibitor in MGC-803 and HGC-27 cells, with β-actin and U6 as internal control, respectively. (B) CCK-8 assay to assess cell viability in response to si-EED and miR-338-5p inhibitor. (C) Colony formation assay to assess the cell colony formation in response to si-EED and miR-338-5p inhibitor. (D) Transwell assay to assess the number of invaded cells in response to si-EED and miR-338-5p inhibitor. Measurement data are expressed as mean ± standard deviation. * p

Figure 3. EED silencing upregulates miR-338-5p to restrain the proliferation and invasion of GC cells. (A) RT-qPCR to examine EED, miR-338-5p expression in response to si-EED and miR-338-5p inhibitor in MGC-803 and HGC-27 cells, with β-actin and U6 as internal control, respectively. (B) CCK-8 assay to assess cell viability in response to si-EED and miR-338-5p inhibitor. (C) Colony formation assay to assess the cell colony formation in response to si-EED and miR-338-5p inhibitor. (D) Transwell assay to assess the number of invaded cells in response to si-EED and miR-338-5p inhibitor. Measurement data are expressed as mean ± standard deviation. * p < 0.05. Data comparison among multiple groups was performed using one-way ANOVA with Tukey's post hoc test. Data comparison between groups at different time points was performed using two-way ANOVA or repeated-measures ANOVA with Bonferroni post hoc test. Cell experiments were repeated 3 times independently.