Figure 5

ERK/ SRC/ CD133 is an indispensable complex for the regulation of N-cadherin. (A) N-cadherin expression decreased dynamically after ERK1/2 inhibitor (10 μg/mL) treatment in Capan1M9 cells, as shown by Western blot analysis. (B) N-cadherin expression decreased dynamically after SRC inhibitor (10 μg/mL) treatment in Capan1M9 cells, as shown by Western blot analysis. (C) N-cadherin expression did not increase following EGF (10 μg/mL) treatment in shCD133M9 cells, although it did increase in shSlugM9 cells following EGF (10 μg/mL) treatment, as shown by Western blot analysis. (D) After transducing His-CD133 into Panc-1 and Capan1M9 cells, anti-His immunoprecipitates (IPs) were probed with anti-ERK1/2, anti-SRC, and anti-CD133 antibodies. IB, immunoblotting. (E) Hypothetical scheme of the CD133/ERK/N-cadherin regulation loop in pancreatic cancer metastasis. CD133 expression was upregulated, and CD133 combined with ERK and SRC to form a regulation complex that was indispensable for EGF activation of the ERK pathway and subsequent N-cadherin expression. CD133 acts as a mesenchymal mediator to facilitate the EMT program.