Fig. 7

SNORA37 promotes gastric cancer progression via facilitating CMTR1-ELAVL1 interplay. a-c Representative images (a and b) and quantification (c) of soft agar and matrigel invasion assays indicating the in vitro growth and invasion of HGC-27 and AGS cells stably transfected with scramble shRNA (sh-Scb) or sh-SNORA37 #1, and those co-transfected with CMTR1 or ELAVL1 (n = 5). d In vivo imaging, growth curve, and weight at the endpoints of xenograft tumors formed by subcutaneous injection of HGC-27 cells stably transfected with sh-Scb or sh-SNORA37 #1, and those co-transfected with CMTR1 or ELAVL1 into dorsal flanks of nude mice (n = 5 for each group). e and f Representative images (e) and quantification (f) of immunohistochemical staining showing the intertumoral expression of CD31 and Ki-67 (brown, arrowheads) within subcutaneous xenograft tumors of nude mice formed by HGC-27 cells stably transfected with sh-Scb or sh-SNORA37 #1, and those co-transfected with CMTR1 or ELAVL1 (n = 5 for each group). g and h Hematoxylin & eosin (HE) staining (g), representative images (h, left panel) and quantification (h, middle panel) of lung metastatic colonization (arrowheads) and Kaplan–Meier curves (h, right panel) of nude mice treated with tail vein injection of HGC-27 cells stably transfected with sh-Scb or sh-SNORA37 #1, and those co-transfected with CMTR1 or ELAVL1 into tail vein of nude mice (n = 5 for each group). One-way analysis of variance (ANOVA) was used to compare the difference in c, d, f, and h. Log-rank test was used for survival comparison in h. *P < 0.05, ** P < 0.01, *** P < 0.001. Data are shown as mean ± SEM (error bars) and representative of three independent experiments in a-c