Fig. 2: Cells lacking miR-200s display significant G1/S cell cycle arrest.
From: Complete loss of miR-200 family induces EMT associated cellular senescence in gastric cancer
A The proliferation of three AGS clones as indicated was measured by EdU. B Soft agar assays. Scale bar, 100 μm. C Western blot analysis of cell cycle-related proteins with β-Actin as the loading control. D Flow cytometry analysis of cell cycle distribution of indicated clones. E The percentage of cycle distribution was shown among three clones. F Tumor sizes of cell-derived xenografic bearing A-NTC, A-31, and A-26 clonal cells were measured twice weekly (n = 4 mice in each group). G Tumor weights were measured at the experimental end-point (tumor volume exceeds 1000 mm3). H Representative images of xenografic tumors inoculated by subcutaneous injection of indicated clones in NSG mice were shown. (I, K, M, O) Representative images of xenografic tumors that were subjected to p21, p53, p-RB, and p-γH2AX staining were shown. Scale bar, 200 μm. (J, L, N, P) The percentage of positive cells for p21, p53, p-RB, and p-γH2AX was depicted. Data in A, B, C, E, J, L, N, and P are presented from triplicate analyses as the mean ± SEM. *p < 0.05, **p < 0.01 and ***p < 0.001.
