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. 2011 Jul 4;208(7):1351–1358. doi: 10.1084/jem.20100951

Figure 3.

Figure 3.

Drug-induced tumor shrinkage causes up-regulation of a Bim transcriptional reporter and elevated Bim protein in tumor-associated ECs. TK-expressing B16.F1 melanomas were grown and treated as described in Generation of B16.F1 and 3LL-LLC cell lines stably expressing TK-SR39 TK. (A) Representative histograms depict EC populations with high β-galactosidase (β-gal) activity. Solid lines depict β-galactosidase activity in ECs from saline-treated tumors, dashed lines depict β-galactosidase activity in ECs from GCV-treated tumors, and closed regions represent a no-FDG negative control. (B) Bar graph depicting the percentages of tumor-associated ECs with high levels of β-galactosidase activity. Data represent the mean ± SEM (n = 3–5 for both saline and GCV treatments). (C) Tumor-associated ECs were purified from >10 WT mice treated twice with saline or GCV and assessed for Bim expression. HSP70 served as a loading control, and the lysate from an Eµ-myc lymphoma served as a positive (+) control. Black lines indicate that intervening lanes have been spliced out.