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. Author manuscript; available in PMC: 2016 Mar 19.
Published in final edited form as: Oncogene. 2014 Apr 14;34(12):1542–1552. doi: 10.1038/onc.2014.89

Figure 5. δ-Catenin truncation variant promotes overgrowth in vitro and in vivo.

Figure 5

(A). δ-Catenin truncation variant promotes overgrowth. The numbers of Rv/C, Rv/δ, and Rv/M1 cells were counted without fresh FBS replenishment after full confluence of cultures. *: p<0.05. (B). Myc-induced tumor development was increased in mutant mice expressing a δ-catenin exon 9 disruption cassette. Inserts: mouse prostates. 400 ×. (C). Histological analysis of No Myc/δ-/- mouse prostate exhibits 1 to 2 layers of epithelial cells, characteristic of normal-appearing prostate glands. Magnification: 100×. Insets: 400×. DLP: Dorsal lateral prostate. VP: Ventral prostate. (D). Quantifications of proliferative and apoptotic cells following immunostaining with anti-Ki67, a marker of cell proliferation, and TUNEL assay, which detects cells undergoing apoptosis in 6-month old mice bearing ARR2PB-driven Myc expression with various δ-catenin expression background. Note that the number of Ki67 positive proliferative cells is dramatically increased and approximately four-fold greater than that for TUNEL staining in Myc/δ-/-. Values represent mean ± S.E.M for a total of 500 cells counted from 2 sets of independent experiments. p< 0.01 * relative to wild type (No Myc/δ+/+) Ki67 and TUNEL.