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Figure 1

Figure 1. A. C. HMGA1 mRNA. Migration. Invasion. 1.0 + 0.001. Control HMGA1. Control HMGA1. Control HMGA1. HMGA1 β -actin. B. Control HMGA1. D. E. HMGA1 Exogenous Endogenous β -actin. Foci #. Absorbance. Control HMGA1

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Figure 1

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  1. Figure 1 A C HMGA1 mRNA Migration Invasion 1.0 + 0.001 Control HMGA1 Control HMGA1 • Control HMGA1 HMGA1 β-actin B Control HMGA1 D E HMGA1 Exogenous Endogenous β-actin Foci # Absorbance Control HMGA1 BxPC-3 MiaPaCa-2 Control HMGA1 1 2 3 4 5 DAYS

  2. Figure 2 A B HMGA1 antibody Histone H3 + Control IgGNegative Control No Chromatin Negative Control No DNA PCR Negative Control XPA-3 HPAF-II 1.0 ± 0.12 1.9 ± 0.46 2.000 PL45 1.10 Relative binding Relative binding HMGA1 antibody Histone H3 +control IgG Negative Control No Chromatin Negative Control No DNA PCR Negative Control HMGA1 antibody Histone H3 + Control IgG Negative Control No Chromatin Negative Control No DNA PCR Negative Control

  3. Figure 3 A XPA-3 PL45 COX-2 mRNA 72 h 72 h HMGA1 mRNA B HMGA1 mRNA HMGA1 Control Knock-down HMGA1 Control Knock-down COX-2 mRNA COX-2mRNA Control HMGA1 HMGA1 Control Knock-down HMGA1 Control Knock-down

  4. Figure 4 A B Control Sulindac Celecoxib

  5. Supplementary Figure 1 HMGA1mRNA PL45 XPA-3 HPAF-II • HMGA1 expression is increased in pancreatic cancer cell lines. • HMGA1 mRNA is increased in pancreatic cancer cell lines. We previously reported that HMGA1 mRNA is increased in XPA-3 and PL-1 cells compared to normal pancreatic tissue (ref. 10.) Here, we show that HMGA1 mRNAis also increased in PL45 and HPAF-II cells.

  6. Supplementary Figure 2 24 h XPA-3 HMGA1 mRNA 48 h COX-2 mRNA HMGA1 Control Knock-down HMGA1 Control Knock-down HMGA1 mRNA HMGA1 Control Knock-down Knock-down of HMGA1 results in repression of COX-2 mRNA levels in XPA-3 cells. COX-2 mRNA levels are repressed in the XPA-3 cells after knock-down of HMGA1 with siRNA (20 nmol/L; Dharmacon) compared with XPA-3 cells treated with the control siRNA (20 nmol/L siCONTROL nontargeting siRNA pool; Dharmacon). The mRNA levels for HMGA1 and COX-2 were normalized to ß-actin (ß-actin primer/probe set; Applied Biosystems) as a loading control, The control treated cells were arbitrarily assigned a value of 1.0. COX-2 mRNA HMGA1 Control Knock-down

  7. Supplementary Figure 3 24 h HMGA1 mRNA PL45 COX-2 mRNA HMGA1 Control Knock-down 48 h HMGA1 mRNA HMGA1 Control Knock-down HMGA1 Control Knock-down Knock-down of HMGA1 results in repression of COX-2 mRNA in PL45 cells. COX-2 mRNA levels are repressed in the PL45 cells after knock-down of HMGA1 with siRNA (20 nmol/L; Dharmacon) compared with PL45 cells treated with the control siRNA (20 nmol/L siCONTROL nontargeting siRNA pool; Dharmacon). The mRNA levels for HMGA1 and COX-2 were normalized to ß-actin (ß-actin primer/probe set; Applied Biosystems) as a loading control. The control treated cells were arbitrarily assigned a value of 1.0. COX-2 mRNA HMGA1 Control Knock-down

  8. Supplementary Figure 4 % Relative Tumor Volume • Control SulindacCelecoxib Tumor volumes are significantly reduced in mice treated with COX-2 inhibitors. Tumor volumes were measured as previously described (ref. 26). The average tumor volume for the control mice in each experiment was considered 100%. Note the significant decrease in tumor volume in mice treated with sulindac (p = 0.010) or celecoxib (p = 0.011) by student’s t-test.

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