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. Author manuscript; available in PMC: 2014 Nov 14.
Published in final edited form as: Gastroenterology. 2012 Oct 3;144(1):134–144.e6. doi: 10.1053/j.gastro.2012.09.061

Figure 6. HH signaling cooperates with PDGFRA signaling in cellular transformation.

Figure 6

(A) Quantification of anchorage-independent clonogenic growth of human non-tumorigenic HaCaT keratinocytes after activation of either HH signaling (by overexpression of GLI1) or KIT signaling (overexpression of the constitutively active Kit D816V mutant) with or without stimulation of PDGFR signaling by PDGFB. Either signal alone has little or no activity towards cellular transformation, whereas GLI1 in combination with PDGFB treatment, but not in combination with KIT activation, leads to formation of clonogenic colonies (spheres) in 3D cultures (asterisks indicate p<0.03 by unpaired t-test). (B) PDGFRA signaling in HaCaT cells after incubation with PDGFB. Western blot analysis shows activation of PDGFRA/ERK/JUN signaling in response to PDGFB treatment.