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1.
Fig. 2

Fig. 2. From: Chemoprevention of Pancreatic Cancer: Characterization of Par-4 and its Modulation by 3,3? Diindolylmethane (DIM).

PAR-4 expression is up-regulated by B-DIM. (A) Western blot analysis of lysates of L3.6pl cells treated with: DMSO (untreated; Lane 1); 10 μmol/L B-DIM (Lane 2); 20 μmol/L (Lane 3), respectively. (B) Western blot analysis of lysates of Colo-357 cells treated with DMSO (untreated; Lane 1); 10 μmol/L B-DIM (Lane 2); 20 μmol/L (Lane 3), respectively. β-actin protein was used as loading control as shown for each blot.

Asfar Sohail Azmi, et al. Pharm Res. 2008 September;25(9):2117-2124.
2.
Fig. 4

Fig. 4. From: Chemoprevention of Pancreatic Cancer: Characterization of Par-4 and its Modulation by 3,3? Diindolylmethane (DIM).

Evaluation of cell viability in B-DIM-treated Colo-357, L3.6pl and BxPC-3 cells by trypan blue staining. Cells were either untreated (DMSO) or treated with increasing concentration of B-DIM (10 and 20 μmol/L) for 96 h and then analyzed for viable cells by trypan blue staining assay as described under MATERIALS AND METHODS.

Asfar Sohail Azmi, et al. Pharm Res. 2008 September;25(9):2117-2124.
3.
Fig. 3

Fig. 3. From: Chemoprevention of Pancreatic Cancer: Characterization of Par-4 and its Modulation by 3,3? Diindolylmethane (DIM).

PAR-4 expression is up-regulated by B-DIM in combination with gemcitabine. (A) Western blot analysis of lysate extracted from Colo-357 cells treated with; DMSO (untreated; Lane 1); B-DIM 20 μmol/L (Lane 2); Gemcitabine 100 nmol/L (Lane 3); B-DIM 20 μmol/L+Gemcitabine 100 nmol/L, respectively. (B) Western blot analysis of lysate extracted from L-3.6pl cells treated with; DMSO (untreated; Lane 1); B-DIM 20 μmol/L (Lane 2); Gemcitabine 100 nmol/L (Lane 3); B-DIM 20 μmol/L+Gemcitabine 100 nmol/L, respectively. Western blot analysis of lysate extracted from BxPC-3 cells treated with; DMSO (untreated; Lane 1); B-DIM 20 μmol/L (Lane 2); Gemcitabine 100 nmol/L (Lane 3); B-DIM 20 μmol/L+ Gemcitabine 100 nmol/L, respectively. Cell lysates were prepared according to the procedure described under MATERIALS AND METHODS section.

Asfar Sohail Azmi, et al. Pharm Res. 2008 September;25(9):2117-2124.
4.
Fig. 1

Fig. 1. From: Chemoprevention of Pancreatic Cancer: Characterization of Par-4 and its Modulation by 3,3? Diindolylmethane (DIM).

Western blot analysis of PAR-4 protein expression in pancreatic cancer cell lines. Panc-1 (Lane 1), L3.6pl (Lane 2), Colo-357 (Lane 3), MiaPaCa (Lane 4), BxPC-3 (Lane 5) and Hs766T (Lane 6). β-actin protein was used as protein loading control as shown for each blot. Cell extracts were prepared according to the procedure described under MATERIALS AND METHODS section.

Asfar Sohail Azmi, et al. Pharm Res. 2008 September;25(9):2117-2124.
5.
Fig. 6

Fig. 6. From: Chemoprevention of Pancreatic Cancer: Characterization of Par-4 and its Modulation by 3,3? Diindolylmethane (DIM).

Sensitization of pancreatic cancer cells, (1) Colo-357, (2) L3.6pl and (3) BxPC-3 to B-DIM (20 μmol/L) and (A) Gemcitabine (Gz) or (B) cisplatin-induced apoptosis as determined by ELISA after 96 h pretreatment with B-DIM (20 μmol/L) alone or a combination of B-DIM (48 h) followed by gemcitabine/cisplatin for 48 h. Increased apoptotic response was evident in combination treatment group of the cells relative to untreated control or individual treatment groups. Each point represents average of 4–5 independent experiments.

Asfar Sohail Azmi, et al. Pharm Res. 2008 September;25(9):2117-2124.
6.
Fig. 7

Fig. 7. From: Chemoprevention of Pancreatic Cancer: Characterization of Par-4 and its Modulation by 3,3? Diindolylmethane (DIM).

(A) and (B) Western blot analysis of PARP, anti-apoptotic Bcl-xl, Bcl-2, p-Akt and the pro-apoptotic Bax in whole cell lysates of L3.6pl and Colo-357 cells after treatment with either only B-DIM (48 h), gemcitabine (48 h), or B-DIM pretreatment (48 h) followed by gemcitabine treatment (48 h). Down-regulation of anti-apoptotic markers is evident in both cell types pre-sensitized with B-DIM followed by gemcitabine treatment. β-actin protein was used as protein loading control as shown for each blot. Cell extracts were prepared according to the procedure described under MATERIALS AND METHODS section.

Asfar Sohail Azmi, et al. Pharm Res. 2008 September;25(9):2117-2124.
7.
Fig. 5

Fig. 5. From: Chemoprevention of Pancreatic Cancer: Characterization of Par-4 and its Modulation by 3,3? Diindolylmethane (DIM).

Sensitization of pancreatic cancer cells, (1) Colo-357, (2) L3.6pl and (3) BxPC-3 to B-DIM (20 μmol/L) and (A) Gemcitabine (Gz) or (B) cisplatin-induced cell growth inhibition as determined by MTT assay after 96 h treatment with B-DIM (20 μmol/L) alone or a combination of B-DIM (48 h) followed by Gemcitabine or cisplatin for 48 h. Increased growth inhibition was evident in combination treatment group relative to untreated control or individual treatment groups. Each point represents average of 4–5 independent experiments.

Asfar Sohail Azmi, et al. Pharm Res. 2008 September;25(9):2117-2124.

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