Fig. 4

GTSE1 promoted breast cancer cell growth by activating AKT pathway. a Decreased expressions of GTSE1 were confirmed by Western blotting in GTSE1-silenced MDA-MB-231 and MDA-MB-468 cells compared with negative control siRNA cells, and GTSE1 overexpression level in MDA-MB-231 and MCF7 cells was validated by immunoblotting. b Cell growth rates were measured by the MTS assay. c Tumor masses isolated from MCF7 stably overexpressing GTSE1 or vector after tumors had grown for 5 weeks. d Overexpression of GTSE1 significantly promoted xenograft tumor volume in female nude mice the final tumor weights. *p < 0.05, **p < 0.01, ***p < 0.001, Student’s t-test. The data are presented as the mean ± S.D. (n = 5 per group) e Stable decreased expression of GTSE1 was confirmed by immunoblotting in GTSE1 silenced MDA-MB-231 cells compared with scrambled shRNA control cells. f The colony formation assays were performed in GTSE1 stably knockdown and control cells to detect the effect of growth. The data are presented as the mean ± S.D. **p < 0.01, Student’s t-test. (from triplicates). g Tumor masses collected from MDA-MB-231 stably expressing Ctr or GTSE1 shRNA after tumors had grown for 22 days. h Knockdown of GTSE1 significantly reduced xenograft tumor growth and volume in female nude mice. i Compared to the negative control shRNA, the final tumor weights were decreased significantly. ***p < 0.001, Student’s t-test. The data are presented as the mean ± S.D. (n = 5 per group). j Phosphorylated and total AKT level in human breast cancer MDA-MB-231 and MDA-MB-468 cells silencing GTSE1 or negative control siRNA, and MDA-MB-231 and MCF7 cells stably expressing a control vector or GTSE1 were determined by immunoblotting. k and l Plate clone formation assays were conducted in the indicated cell lines after a specific AKT inhibitor LY294002 treatment