Supplementary Figure Legend from FOXM1c Promotes Pancreatic Cancer Epithelial-to-Mesenchymal Transition and Metastasis via Upregulation of Expression of the Urokinase Plasminogen Activator System

Supplementary Figure Legend from FOXM1c Promotes Pancreatic Cancer Epithelial-to-Mesenchymal Transition and Metastasis via Upregulation of Expression of the Urokinase Plasminogen Activator Syste

Supplementary Materials and Methods from FOXM1c Promotes Pancreatic Cancer Epithelial-to-Mesenchymal Transition and Metastasis via Upregulation of Expression of the Urokinase Plasminogen Activator System

Supplementary Materials and Methods: 1. Cell scratch-wound assay. 2. Cell migration assay. 3. Cell invasion assay. 4. Animals. 5. Experimental liver metastases. 6. Western blot analysis.</p

9 Supplementary Figures from Krüppel-like Factor 4 Suppresses Serine/Threonine Kinase 33 Activation and Metastasis of Gastric Cancer through Reversing Epithelial–Mesenchymal Transition

9 Supplementary Figures: Supplementary Figure S1. Immunohitochemical analysis of STK33 in TMAs of gastric cancer tissue specimens with different differentiation grade. Supplementary Figure S2. Estimates of OS and DFS of gastric cancer patients from GSE66229 (N=300). Supplementary Figure S3. STK33 expression patterns in human gastric cancer tissues and cell lines. Supplementary Figure S4. Effect of altered STK33 expression on gastric cancer metastasis and EMT. Supplementary Figure S5. Effect of altered STK33 expression on gastric cancer growth in vitro and in vivo. Supplementary Figure S6. Identification of STK33 as a downstream target gene of KLF4. Supplementary Figure S7. KLF4 negatively regulated STK33-induced invasion and EMT. Supplementary Figure S8. Identification of transcriptional inhibition on STK33 expression by KLF4 in pancreatic cancer cells. Supplementary Figure S9. STK33 kinase inhibitor BRD-8899 failed to inhibit STK33-induced cell proliferation, migration and invasion in GC.</p

7 Supplementary Tables from Krüppel-like Factor 4 Suppresses Serine/Threonine Kinase 33 Activation and Metastasis of Gastric Cancer through Reversing Epithelial–Mesenchymal Transition

7 Supplementary Tables: Supplementary Table S1. Clinicopathologic characteristics of the 625 GC patients from whom the TMA specimens were obtained Supplementary Table S2. Clinicopathologic characteristics of the 45 GC patients from whom the TMA specimens were obtained Supplementary Table S3. The sequences of the gene-specific primers used in real-time PCR analysis, vector constructs, and ChIP analysis Table S4. Expression of STK33 in Normal Mucosa, Intraepithelial Neoplasia and Gastric Cancer Table S5. Relation between STK33 Expression and Clinicopathological Parameters in Patients with Gastric Cancer Table S6. Univariate Cox Regression Analysis of Factors Associated With Overall Survival in Gastric Cancer Patients Table S7. Multivariate Cox Regression Analysis Of Factors Associated With Overall Survival in Gastric Cancer Patients</p

Supplementary Figure 1 from FOXM1c Promotes Pancreatic Cancer Epithelial-to-Mesenchymal Transition and Metastasis via Upregulation of Expression of the Urokinase Plasminogen Activator System

Supplementary Figure S1. Influence of altered expression of FOXM1 isoforms on pancreatic tumor cell migration and invasion.</p

The receptors by which NE and IFN-γ affect MHC-I, B7-1, IDO and B7-H1 expression.

<p>NE exerted its effects on MHC-I (A), IDO (C) and B7-H1 (D) expression mainly through the β₂ adrenergic receptor and on B7-1 (B) through the α₂ adrenergic receptor. (* Significant difference from control group, P<0.05; # Significant difference from NE group (10⁻⁶ M), P<0.05; $ Significant difference from NE/IFN-γ group, P<0.05; & Significant difference from IFN-γ group (100 ng/mL), P<0.05).</p

The effect of NE/IFN-γ on MHC-I, B7-1, IDO and B7-H1 expression in MIA PaCa-2 (A and B) and BxPC-3 cell lines (C and D).

<p>Compared with control group, NE suppressed MHC-I and B7-1 and up-regulated IDO and B7-H1 in a dose-dependent manner. IFN-γ suppressed B7-1, and up-regulated IDO and B7-H1. Compared with NE group, NE and IFN-γ had significant synergistic effects on IDO and B7-H1 (B and D).</p

Time-dependent effects of NE/IFN-γ on MHC-I (A), B7-1 (B), IDO (C) and B7-H1 (D) mRNA expression.

<p>NE/IFN-γ had time-dependent suppressive effects on MHCI and B7-1 and stimulatory effects on IDO and B7-H1 expression. When NE (10⁻⁶ M), IFN-γ (100 ng/mL) or NE (10⁻⁶ M) plus IFN-γ (100 ng/mL) was removed after 48 hours, the residual effects decreased dramatically within 1 week.</p

The effects of NE/IFN-γ on MHC-I, B7-1, IDO and B7-H1 protein expression.

<p>Western blot results are shown on the left and at the top; histograms depicting relative intensities are shown on the right and at the bottom (A and B). Immunohistochemical staining of MIA PaCa-2 cells is shown at 400×magnification (C).</p

Dose-dependent effects of NE/IFN-γ on the proliferation and invasion of PC cells.

<p>NE and IFN-γ affect proliferation (OD 490 nm) and invasion (OD 570 nm) of MIA PaCa-2 (A and B) and BxPC-3 (C and D) cells in a dose-dependent manner. Low concentrations of NE (10⁻⁸ M) exhibited a trend toward stimulation, while NE (10⁻⁶ M) exhibited a trend toward suppression (<i>P</i>>0.05). High concentrations of NE (10⁻⁵ M) and IFN-γ (100 ng/mL, 200 ng/mL) had significant suppressive effects (<i>P</i><0.05). A β₂-AR antagonist decreased the stimulatory effects of NE (10⁻⁸ M) but did not alter the suppressive effects of NE (10⁻⁶ M) (E and F). (* Significant difference with control group, <i>P</i><0.05).</p