Fig. 4

ITGA2 promoted tumor growth in pancreatic cancer in vivo. a and b. PANC-1 cells were infected with sh-Control, sh-ITGA2, or sh-ITGA2 and ITGA2 plasmid. The cells were harvested for RT-PCR analysis (a) and Western blot analysis (b). GAPDH served as an internal reference. sh-Control group was compared with sh-ITGA2 group, sh-ITGA2 group was compared with sh-ITGA2 + ITGA2 group. Statistical analyses were performed with one-way ANOVA followed by Tukey’s multiple comparison’s tests. ***, P < 0.001. c and d. PANC-1 cells infected with sh-Control, sh-ITGA2, or sh-ITGA2 and ITGA2 plasmid were harvested for colony formation assay (c) and MTS assay (d) after forty-eight hours culturing. Each bar represents the mean ± SD of three independent experiments. sh-Control group was compared with sh-ITGA2 group, sh-ITGA2 group was compared with sh-ITGA2 + ITGA2 group. Statistical analyses were performed with one-way ANOVA followed by Sidak’s multiple comparison’s tests. **, P < 0.01. e-g. After 72 h postinfection, PANC-1 cells infected with sh-Control, sh-ITGA2, or sh-ITGA2 and ITGA2 were subcutaneously injected into nude mice. The tumors were harvested and photographed (e) on day 21. Data on tumor volume (f) and tumor mass (g) were shown as means ± SD (n = 5). sh-Control group was compared with sh-ITGA2 group, sh-ITGA2 group was compared with sh-ITGA2 + ITGA2 group. Statistical analyses were performed with two-way ANOVA followed by Sidak’s multiple comparison’s tests. ns, not significant; ***, P < 0.001. h. IHC analysis for Ki-67 expression was performed in tumors harvested from xenografts, and percents of the Ki-67 positive cells were quantified. All data were shown as mean ± SD (n = 5). sh-Control group was compared with sh-ITGA2 group, sh-ITGA2 group was compared with sh-ITGA2 + ITGA2 group. Statistical analyses were performed with one-way ANOVA followed by Tukey’s multiple comparison’s tests. *, P < 0.05; **, P < 0.01