| Popis: |
Supplementary Figure 1. (a) Representative images of metastasis to the liver of control mice in Colo357 model was shown by H&E staining. Total magnifications are 100X and 200X. Scale bar, 50μm. (b) Colo357 human pancreatic cancer cells (1 × 106) were injected orthotopically into the pancreas of SCID mice. Treatment began when the established tumor was visible by ultrasound, and consisted of control (saline, n = 6), gemcitabine 25 mg/kg twice weekly plus erlotinib 100 μg daily (standard of care, n = 6) as described in Kirane et al. (29), or mcr84 plus apricoxib (n = 10) and continued for 3 weeks. Tumor weight was normalized to the control and data from the treatment groups were compared. Data are displayed as mean {plus minus} SEM. *P < 0.05 vs. control, by ANOVA with Dunn's MCT. Supplementary Figure 2. Human pancreatic cancer cell lines, Colo357 (a) and AsPc-1 (b) were plated either under normal conditions or under conditions of forced EMT (treated with 20 ng/mL TGFβ on collagen I -coated plates for 72 hours). PGE2 levels were measured by ELISA after 500 nM apricoxib treatment. (c) Colo357 and AsPC-1 cells were plated under normal conditions or conditions of forced EMT (50 ng/ml TGFβ on collagen I -coated plates for 24 hours). Lysates were probed for the indicated targets by Western blotting. The induced EMT conditions promoted loss of E-Cadherin, gain of Vimentin expression. In Colo357, the expression of N-Cadherin was also upregulated by collagen I and TGFβ stimulation. β-actin was used as a loading control. Supplementary Figure 3. Microvessel density is not decreased by COX-2 inhibition. Supplementary Figure 4. KIC pancreatic tissues from the treated mice were subjected to immunohistochemistry Supplementary Figure 5. Anti-VEGF therapy results in reduced microvessel density, hypoxia induced TGFβ expression, epithelial plasticity and enhanced collagen deposition Table S1: List of antibodies |
