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. 2000 Jul 5;97(14):7748–7753. doi: 10.1073/pnas.97.14.7748

Figure 3.

Figure 3

BRG-1 deficiency renders tumor cell lines resistant to RB-mediated signaling and arrest. (A) Thirty micrograms of total protein from MCF-7, PANC-1, U87, SW13, PC3, C33A, SAOS-2, U2OS, and RD was separated by 7.5% SDS/PAGE and immunoblotted for BRG-1 and actin. (B) MCF-7, PANC-1, SW13, U87, PC3, C33A, SAOS-2, U2OS, and RD were cotransfected with GFP expression plasmid and either vector or PSM-RB. Cells were labeled with BrdUrd, and the percentage of inhibition of BrdUrd incorporation by PSM-RB relative to vector is reported. The data for MCF7, U87, PC3, RD, and U2OS have been previously published (25) and are shown for illustrative purposes. (B) SW13 cells were cotransfected with H2B-GFP expression plasmid and plasmids encoding vector, PSM-RB, p16ink4a, or p27Kip1. Cells were labeled with BrdUrd, and the percentage of transfected cells incorporating BrdUrd is shown. (C) SW13 cells were transfected with E2F/Luc, CMV-β-gal, and PSM-RB plasmids. SW13 cells were also transfected with the cyclin A promoter reporter plasmid −608Luc, CMV-β-gal, and PSM-RB. (D) SW13 and PC3 cells were cotransfected with either vector, p16ink4a, or PSM-RB along with pBabe-PURO. Twenty-four hours after transfection, cells were subjected to puromycin selection. Selected cells were harvested, and equal total protein was resolved by SDS/PAGE and then subjected to immunoblot analysis for RB, cyclin A, Cdk2, cyclin E, and Cdk4 protein.