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. Author manuscript; available in PMC: 2009 Oct 1.
Published in final edited form as: Mol Cancer Ther. 2008 Oct;7(10):3363–3372. doi: 10.1158/1535-7163.MCT-08-0439

Figure 4. Activation of ER stress and pro-apoptotic pathways by C-DIM compounds in pancreatic cancer cells.

Figure 4

(A) Induction of ER stress and apoptosis in Panc-1 cells. Panc-1 cells were treated with DMSO (D), 15 μM DIM-C-pPhBr or DIM-C-pPhF (P) or their corresponding N-methyl analogs (N) for 24 hr, and whole cell lysates were analyzed by western blots as described in the Materials and Methods. (B) Concentration- and time-dependent induction of PARP cleavage. Panc1 cells were treated with different concentrations of DIM-C-pPhBr (for 24 hr) or treated with DIM-C-pPhBr and DIM-C-pPhF for different times. Whole cell lysates were analyzed for cleaved PARP by Western blots as described in the Materials and Methods. Induction of ER stress (C) and apoptosis (D) by DIM-C-pPhBr and related compound in pancreatic cancer cells. Panc-28, BxPC3, MIAPaCa-3 and L3.6pl cells were treated and analyzed by western blots essentially the same as described in A/B above. β-Tubulin served as a loading control for all experiments and the blots illustrated in A–D were observed in 2 or more separate experiments.