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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

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


Figure 1

  • 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


Figure 1

  • 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


Figure 1

Figure 4

A

B

Control

Sulindac

Celecoxib


Figure 1

  • 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.


Figure 1

  • 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


Figure 1

  • 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


Figure 1

  • 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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