Fig. 7
DAB2 regulates gastric tumorigenesis in a YAP1-dependent manner. A-C HGC27 cells with/without DAB2 knockdown were serially diluted and xenografted into nude mice subcutaneously. (A-B) The tumor cell numbers injected and frequency of tumor formation at day 35. (C) The probability estimates calculated with Extreme Limiting Dilution Analysis (ELDA) software (http://bioinf.wehi.edu.au/software/elda/). A significant difference in tumor formation capacity was observed between the control and shDAB2 groups. D Tumor weight for subcutaneous tumor xenografts with shRNA knockdown or control (1 million cells dose group); **P < 0.01. E Western blot for DAB2 and its downstream signaling genes for xenograft tumors with/without DAB2 silencing (from 1 million cells dose group). F-G Tumour growth curves of Scramble-vector, Scramble-OE, shYAP1-vector, and shYAP1-OE groups were shown. ***P < 0.001. H Representative IF images (magnification ×100, scale bars, 100 μm) of DAB2, active-YAP1, and p-STAT3 in human adjacent normal tissue and tumor; nuclei were stained with DAPI (blue). I Representative IF images (magnification×100, scale bars, 100 μm) of active-YAP1 and Ki-67 in human DAB2high and DAB2low GC tissues; nuclei were stained with DAPI (blue). J The quantification of nuclear Ki67 fluorescence is shown as the mean ± standard deviations of DAB2high and DAB2low GC tissues; **P < 0.01. K-L Kaplan-Meier survival curve indicates that GC patients with high expression of DAB2 (K) and DAB2 + active-YAP1 (L) have poor overall survival (OS) compared with GC patients with low expression. HR, hazard ratio