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. 2017 Apr 27;8(26):42728–42741. doi: 10.18632/oncotarget.17449

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Copyright: © 2017 Yu et al.

This article is distributed under the terms of the Creative Commons Attribution License (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited.

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(A) The remaining cells viabilities after VIP incubation and CPT induced apoptosis by MTT assay showed that the viabilities remained of the VPAC1-CHO cells was significantly higher than that of VPAC1-C37/A-CHO cells (*P < 0.01, VPAC1-CHO vs. VPAC1-C37/A-CHO). The data were means ± SEM of six experiments. (B) The plasma anti-apoptotic protein Bcl-2 levels after VIP incubation and CPT induced apoptosis showed that VPAC1-CHO cells had significant higher Bcl-2 levels than VPAC1-C37/A-CHO cells (*P < 0.01, VPAC1-CHO vs. VPAC1-C37/A-CHO). The data were means ± SEM of six experiments. (C) The anti-apoptotic viabilities in VPAC1-CHO and VPAC1-C37/A-CHO by flow cytometry assay in CPT induced apoptosis showed that the apoptotic percentage of VPAC1-CHO (3.6% in Q3 quadrant) is significantly lower than that of VPAC1-C37/A-CHO (7.63% in Q3 quadrant). (D) Microscope imaging of VPAC1-CHO and VPAC1-C37/A-CHO cells treated with both VIP (0.1 nM) and CPT (50 uM) and stained by TUNEL assay. It was shown that brown staining in VPAC1-CHO cells was significantly less than VPAC1-C37/A-CHO cells. The statistic analysis on the TUNEL signals showed that VPAC1-CHO cells had significant lower TUNEL signal than VPAC1-C37/A-CHO cells (*P < 0.01, VPAC1-CHO vs. VPAC1-C37/A-CHO.) The data were means ± SEM of four experiments.