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. 2015 Mar 15;29(6):658–671. doi: 10.1101/gad.256628.114

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© 2015 Roy et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 5. — Re-expression of Brg1 in Kras^G12D; Brg1^f/f PDCs and IPMN-derived PDA tumor cells enhances their tumorigenic properties. (A) Western blot showing ectopic expression of Brg1 in IPMN-derived PDA. (B) Brg1 put backs in Kras^G12D; Brg1^f/f PDCs and IPMN-derived PDA show increased anchorage-independent growth compared with Brg1-null cells. (C, left) Western blot depicting ectopic expression of Brg1 in the Brg1-null human PDA cell line Tu8988T. (Right) Soft agar colony formation assay showing that Brg1-null human PDA cell line Tu8988T forms more colonies on soft agar upon ectopic expression of Brg1. Brg1 put backs in IPMN-derived PDA lines (D) and Kras^G12D; Brg1^f/f PDCs (E) were subcutaneously injected into NOD scidγ (NSG) mice and monitored for tumor growth. Mice were sacrificed 4 wk after inoculation, and tumors were excised. Tumor mass and volume are significantly higher in Brg1 put backs. (F) Costaining of Ki67, smooth muscle actin (SMA), cleaved caspase 3, and DAPI of tumors obtained in D. Bars: H&E, 250 μm; Ki67, cleaved caspase 3, and SMA, 100 μm.