Fig. 3

PTBP3 increases colon cancer cells motility and angiogenesis in vitro and in vivo. a Cell migration and invasion of HCT116 cells ± PTBP3 KD/OE, and SW480 cells ± PTBP3 OE measured as percent cells migrating to chambers. b Relative migration fold changes in HCT116 cells ± PTBP3 KD/OE, and SW480 cells ± PTBP3 OE. c Relative invasion fold changes in HCT116 cells ± PTBP3 KD/OE, and SW480 cells ± PTBP3 OE. d HCT116 cells ± PTBP3 KD were injected via the lateral tail veins, respectively. Representative lung images at week 5; corresponding hematoxylin/eosin–stained lung sections are shown. Arrows, lung metastasis foci. e Lung nodules at week 5 were analyzed as the numbers of nodules per mouse. n = 8. f Detection of VEGF protein expression using Western blot in HCT116 cells ± PTBP3 KD/OE. GAPDH was used as a loading control. g-h PTBP3 in CRC cells positively regulated tube formation. Numbers of complete tubular structures formed by HUVECs were counted for ± PTBP3 KD/OE in HCT116 cells. Data are presented as the means ± SD for experiments in triplicate. i Photographs of matrigel plugs with HCT116 cells ± PTBP3 KD excised from mice after 7 days of growth in vivo. j IHC detection of PTBP3, VEGF and CD31 in xenograft tumors formed by HCT116 cells ± PTBP3 KD after 7 days of growth in vivo. Scale bar: 100 μm. k Quantification of CD31 positive microvessel density in tumor xenografts formed by HCT116 cells ± PTBP3 KD. A pool of two independent shRNAs (#1 and #2) was used for PTBP3 KD. Statistical analysis was conducted using a two-tailed student’s t test, Data are presented as the means ± SD for experiments in triplicate. *p < 0.05, **p < 0.01,***p < 0.001