Fig. 3.

αB-Crystallin is required for oncogenic transformation by E1A and inhibits the apoptosis-sensitizing effects of E1A. a WT and αB-crystallin^−/− KO MEFs stably expressing DN p53 and E1A (abbreviated WT E1A DN p53 and KO E1A DN p53) were grown in subconfluent culture with the indicated passage (p) number reflecting 3-day growth periods (mean ± SD, n = 3). b WT E1A DN p53 MEFs and αB-crystallin^−/− KO E1A DN p53 MEFs were grown in soft agar for 2 weeks and the number of colonies was scored (mean ± SD, n = 3). WT and αB-crystallin^−/− KO DN p53 MEFs stably expressing H-RasV12 oncogene were also analyzed. c WT and αB-crystallin^−/− KO E1A DN p53 MEFs were examined for transwell invasion through Matrigel-occluded pores using 10 % FCS as a chemoattractant. Invading cells were visualized by crystal violet staining and scored (mean ± SD, n = 3). d Immortalized WT and αB-crystallin^−/− KO DN p53 MEFs were acutely infected with a retrovirus expressing E1A and the percentage of Annexin V-positive MEFs was determined by flow cytometry (mean ± SD, n = 3). e and f WT E1A DN p53 MEFs and αB-crystallin^−/− KO E1A DN p53 MEFs were treated with 250 nM Taxol (e) or 1 μM Doxorubicin (Dox) (f) for 24 h and the percentage of Annexin V-positive cells was determined (mean ± SD, n = 3). *P < 0.05, **P < 0.01, or ***P < 0.001 versus control WT E1A DN p53 MEFs