Figure 5.

E-cadherin-GFP FRAP during Tissue Homeostasis, Initiation, and Progression of Pancreatic Cancer

(A) Proposed pancreatic cancer progression model from initiating Kras mutations (PanIN) to subsequent loss of p53 or gain-of-function mutations in p53.

(B) Representative whole-body image of an E-cadherin-GFP mouse with multiphoton-based cell-cell junction imaging (inset: E-cadherin-GFP, green; SHG signal, purple).

(C) Representative images from confocal FRAP movies in the E-cadherin-GFP mouse from normal pancreas (first row) to acquiring Kras^G12D (second row) with subsequent loss of p53 (third row) or p53^R172H gain-of function mutations (bottom row), respectively. Red arrows, bleached regions.

(D and E) Graphs comparing E-cadherin-GFP mobilization between in situ pancreatic tissue from normal (green), Kras^G12D alone (blue), Kras^G12D; p53^−/− (purple), and Kras^G12D; p53^R172H (orange) mice. Columns, mean; bars, ± SE, n = 3 mice/group, ≥21 junctions in total. ^∗p < 0.05 (unpaired Student’s t test).

(F) Proposed schematic of E-cadherin dynamics during PDAC progression.

See also Figure S4.