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. Author manuscript; available in PMC: 2019 Sep 1.
Published in final edited form as: Mol Carcinog. 2018 May 8;57(9):1130–1143. doi: 10.1002/mc.22830

Figure 3: The cell kinetic effect of CMC2.24 in pancreatic cancer cells.

Figure 3:

A: AsPC-1 cells treated with CMC2.24 for 24 h were stained with Annexin V/propidium iodide, and the percentage of apoptotic cells was determined by flow cytometry. B: MIA Paca-2, Panc-1 and BxPC-3 cells treated with various concentrations of CMC2.24 for 24 h were stained with Annexin V/propidium iodide, and the percentage of apoptotic cells was determined by flow cytometry. Results are expressed as fold-increase compared with the percentages of apoptotic cells in the control cells. *p<0.05, vs. control. C: Differential cytotoxic effect of CMC2.24 in Panc-1 cells compared with that in HPNE. Apoptosis was determined by flow cytometry in HPNE and Panc-1 cells incubated with or without 55 μM of CMC2.24 for 24h. Results are expressed as fold-increase compared with the percentages of apoptotic cells in the control cells. D: CMC blocks the S/G2 cell cycle phase transition after 24 h treatment in human AsPC-1 and MIA PaCa-2 cells, determined by flow cytometry following propidium iodide staining. E: The percentage of proliferating cells in vehicle or CMC2.24-treated PDTX xenografts were determined by Ki-67 staining. Representative images (x20) of tissue sections from PDTX tumors treated with either vehicle (control) or CMC2.24 and stained for Ki-67 expression (proliferation marker). The proliferation indices of xenograft tumors were determined and expressed as the mean ± SEM.