Fig. 2
From: VAV2 is required for DNA repair and implicated in cancer radiotherapy resistance
Irradiation induces ESCC cell radioresistance by evoking aberrant VAV2 overexpression. a, b Forced VAV2 overexpression in KYSE150 cells (a) or radiosensitive PDC-2 cells (b) caused resistance of cells to IR treatment. Left panels show proliferation curves of cells and right panels shows fractions of cell survival by limiting dilution assays. IR, irradiation (4 Gy). c Silencing VAV2 expression by siRNA in radioresistant PDC-5 cells significantly increased sensitivity of cells to IR treatment. Left panels show proliferation curves of cells with siRNA#1 (the results of siRNA#2 are shown in Supplementary Fig. S2g); middle and right panels show fractions of cell survival by limiting dilution assays. IR, irradiation (4 Gy). d, e Western blot analysis showed overexpression of VAV2 and γ-H2AX in ESCC cells treated with radiation (10 Gy), which is time- (d) and dose-dependent (e). f Comparison of VAV2 mRNA (left panel) and protein (right panel) levels in IR-induced radioresistant KYSE150 cells (KYSE150R) and its parental KYSE150 cells. Results are mean ± SEM from three independent determinations and each had three triplicates. P of Mann–Whitney test. g Tumor spheres of KYSE150 and KYSE150R cells treated with or without radiation (4 Gy). Left panel shows representative images of tumor spheres and right panel shows statistics. Scales bars, 100 μm. Data are mean ± SEM from at least three independent experiments and five fields were randomly selected for each experiment. *P < 0.05; **P < 0.01; ***P < 0.001 and ****P < 0.0001 of Student’s t-test
