Figure 2. (a-d): Inhibition of proliferation and induction of apoptosis in pancreatic cancer and breast cancer: a-b.

Inhibition of cell proliferation using different modified GIPC peptides in (a) AsPC1 cells and (b) MDA-MB-231-WT cells for 48 h. With a [³H]-thymidine incorporation assay, a dose-dependent significant inhibition of cell proliferation was observed in both cell lines when cells were treated with compound CR1166 compared to parent active peptide CR1023. No inhibition was observed with control peptides (CR2055, CR2059), or peptides (CR1162, CR1170) or DMSO. Inhibition of proliferation of AsPC1 cells was significantly increased with increasing concentration of CR1023 and CR1166 peptides. CR1166 is the best peptide for inhibition of cell proliferation in both cell lines compared to CR1023 and the control peptides. AsPC1 cells were incubated with different peptides for 48 hours at different three concentrations (50, 100 and 200 µM). DMSO indicates cells treated with DMSO (required for 200 µM peptides dissolved in DMSO). (c-d). Induction of apoptosis in AsPC-1 and MDA-MB-231-WT cells. Apoptosis assay of (c) AsPC-1 and (d) MDA-MB-231-WT cells treated with DMSO, and compounds CR1023, CR1164, CR1170, CR2055, and CR2059 in a dose-dependent manner (50–200µM) for 48 hours. Significant apoptosis was observed after treatment with CR1023 and CR1166 in both cell lines in a dose-dependent manner. CR1166 is most effective among all peptides. No inhibition was observed with either the control peptide CR2055 or DMSO. Apoptosis assay of AsPC-1 and MDA-MB-231-WT cells treated with DMSO and modified GIPC peptides in a dose-dependent manner (50–200µM) for 48 h of treatment using Annexin V-FITC Apoptosis Kit. Significant induction of apoptosis was observed by compound CR1166.