Fig. 2: Fip200 knockdown decreases vascular tumour cell proliferation, migration and tumorigenicity.

a Lysates from mouse EC or 562 tumour cells treated with control or two separate Fip200 shRNA were examined by western blots with various antibodies as indicated. b–f 562 tumour cells and Fip200-KD cells were measured for cell proliferation (b), ncolony formation (c, d) and migration by wound healing assay (e, f). Data are presented as mean ± SD; n = 3 biologically independent cells. Scale bar in (e), 300 μm. g–l 562 tumour cells and Fip200-KD cells (10⁶ cells) were subcutaneously injected in recipient nude mice. Representative images of tumour formation at injection site at 4 weeks after injection are shown in (g), arrows mark tumour formation at the injection sites of Ctrl (red arrow) and Fip200-KD (blue arrow) mice, and Mean ± SEM of tumour volume are shown in (h). n = 6 biologically independent samples. Representative images of histological analysis by H & E staining, and IHC for CD31, Ki67, pS6RP and cleaved caspase 3 of tumour sections are shown in (i) and (j), respectively. The boxed area with yellow line is magnified. Scale bar, 500 μm (i left panel) and 50 μm (i right panel), 200 μm for CD31, Ki 67 and P-S6RP (S240/244) (j) and 50 μm for cleaved caspase 3 (j). Quantification of Ki67 positive cells per field of view (k) and percentage of cleaved caspase 3+ cells (l) in control and Fip200 KD transplanted tumours are shown as mean ± SD. n = 4 biologically independent samples. m Lysates from 562tumour cells and Fip200-KD cells were examined by immunoblots with various antibodies as indicated. Unpaired two-tailed t test was used in (b, d, f, h, k, and l). Source data are provided as a Source Data file.