Display Settings:

Items per page

Results: 6

1.
Figure 2

Figure 2. TRF2 Induces COX-2 via a Phospho-p38-Dependent Mechanism. From: DNA Damage Drives an Activin A-Dependent Induction of COX-2 in Premalignant Cells and Lesions.

A) Mean COX-2 mRNA levels in untreated parent vHMEC, pWP1, TRF2-vHMEC or hTERT-vHMEC (hatched bars, shown in Figure 1C) or treated with the phospho-p38 inhibitor, SB203580 for 24h (grey bars). B) Representative immunoblot showing COX-2, phospho-p38 (p-p38) and actin (loading control) protein levels for the conditions described in A. C) Mean levels of prostaglandins in conditioned media (left panel). Wounding assay for parent, pWP or TRF2-vHMEC (right panel).

Colleen Fordyce, et al. Cancer Prev Res (Phila). ;3(2):190-201.
2.
Figure 1

Figure 1. DNA Damage Induces COX-2 in vHMEC. From: DNA Damage Drives an Activin A-Dependent Induction of COX-2 in Premalignant Cells and Lesions.

RM9, RM15 and RM16 were used in panels A-C. A) vHMEC were exposed to 100μM Etoposide (top), 60J/m2 UVC (middle) and 0.055μmol/ml NU7026 (bottom) and mean COX-2 mRNA levels were measured at the indicated times. Error bars represent the standard error of the mean. B) COX-2 mRNA levels in early, mid or late passage vHMEC. C) COX-2 mRNA levels in vHMEC infected with lentivirus containing either TRF2 or empty vector (pWP1). D) COX-2 mRNA levels in vHMEC (RM15, RM16, RM18) infected with lentivirus containing either hTERT or empty vector (pWP1). Asterisks indicate statistically significant (p<0.05) changes in expression compared to vector or untreated control.

Colleen Fordyce, et al. Cancer Prev Res (Phila). ;3(2):190-201.
3.
Figure 5

Figure 5. DNA Damage Induces Activin A, COX-2 and Growth Arrest in p16-Competent HMEC. From: DNA Damage Drives an Activin A-Dependent Induction of COX-2 in Premalignant Cells and Lesions.

A) HMEC were exposed to 100μM Etoposide (RM40, RM45, RM46) or to 60J/m2 of UVC (RM45) as described in Figure 1A. Line graphs indicate relative COX-2 and activin A mRNA levels and activin A protein levels in conditioned media compared to the untreated control. B) Activin A, COX-2, p16 and p21 mRNA levels in parent, vector (pWP1) or TRF2-HMEC (CM7, RM146). C) Population doublings in HMEC (CM7) infected with lentivirus containing TRF2 or empty vector (pWP1) or parent HMEC. D) Overview of the DNA damage-dependent COX-2 induction and its consequences in HMEC (intact p16/Rb) or vHMEC (silenced p16).

Colleen Fordyce, et al. Cancer Prev Res (Phila). ;3(2):190-201.
4.
Figure 3

Figure 3. Activin A is Induced by DNA Damage and Coincides with COX-2 Expression. From: DNA Damage Drives an Activin A-Dependent Induction of COX-2 in Premalignant Cells and Lesions.

A) vHMEC (RM9, RM15, RM16) were treated as described in Figure 1A. Line graphs indicate the relative level of COX-2 and activin A mRNAs and activin A protein in conditioned media compared to the untreated control. COX-2 mRNA levels (shown in Figure 1A) are indicated for comparison (light grey dashed line). B) Mean activin A mRNA levels (light grey bars) in vHMEC (RM9, RM15, RM16) and protein levels (dark grey bars) in early, mid and late passage RM9 vHMEC in duplicate experiments. Activin A mRNA (panel C) and protein (panel D) levels in RM9, RM15, RM16 and RM18 vHMEC overexpressing either TRF2, hTERT or vector (pWP) or mock infected (parent).

Colleen Fordyce, et al. Cancer Prev Res (Phila). ;3(2):190-201.
5.
Figure 4

Figure 4. Activin A and p53 are Necessary for COX-2 Induction. From: DNA Damage Drives an Activin A-Dependent Induction of COX-2 in Premalignant Cells and Lesions.

A) Activin A levels were reduced using shRNA. Mean relative COX-2 and activin A mRNA and activin A protein levels measured as described in Figure 3B in RM9, RM15, RM16 and expressed relative to parent (parent, pWP1 or TRF2) or pGL3 (all others). B) COX-2 mRNA levels in vHMEC incubated with exogenous activin A (left panel). Immunoblot showing COX-2, phospho-p38 (p-p38) and actin (loading control) protein levels for each treatment. Conditioned media from parent, vector or TRF2-vHMEC obtained from 2 donors (RM9, 15) was diluted 1:1 and added to vHMEC obtained from 3 donors (RM9, 15, 16). Corresponding immunoblots of treated cells showing COX-2, p-p38 and actin (loading control) expression (right panel). C) ATM and p53 levels were reduced using shRNA. Mean COX-2 and activin A mRNA and activin A protein levels in RM9, RM15 and RM16 expressed relative to parent (parent, pWP1 or TRF2) or pGL3 (all others). For A and C, asterisk (*) indicates statistically significant changes compared to either parent, pGL3 or TRF2+pGL3.

Colleen Fordyce, et al. Cancer Prev Res (Phila). ;3(2):190-201.
6.
Figure 6

Figure 6. Telomere Content is Inversely Associated with TRF2, Activin A and COX-2 Expression in Ductal Carcinoma in Situ (DCIS). From: DNA Damage Drives an Activin A-Dependent Induction of COX-2 in Premalignant Cells and Lesions.

A) γH2AX, TRF2, activin A and COX-2 protein levels were evaluated by immunohistochemistry. Lesions were divided into two groups based on staining intensity for each protein. Telomere content in DCIS lesions was expressed as a percentage of placental DNA. Box plots show the relationship between γH2AX (far left), TRF2 (left), activin (right) and COX-2 (far right) and telomere content in high and low expression lesions. p-values for each comparison are shown in the inset. B) Examples of serial sections for high and low expression DCIS lesions (20x) stained with H&E, and γH2AX, TRF2, activin A and COX-2 antibodies. Nuclei counterstained with hematoxylin (blue) and primary antibodies against each antigen detected using AEC (red). C) Contingency tables showing the number of cases with high or low COX-2 levels versus the number of cases with high or low γH2AX, TRF2 and activin A.

Colleen Fordyce, et al. Cancer Prev Res (Phila). ;3(2):190-201.

Display Settings:

Items per page

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Write to the Help Desk