Skip to main content
Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: NAD pool as an antitumor target against cancer stem cells in head and neck cancer

Fig. 5

Proliferation rate recovery of NAMPT CRISPRs during the growth curve in HNSCC cell lines. A Growth curves of NAMPT CRISPRs and control (empty vector only, EV) cells of RPMI-2650 and Detroit-562 cell lines. B Total NAD and NAD + quantification of NAMPT CRISPRs and (empty vector only, EV) cells at three different points on the growth curve: Day 4, Day 7 and Day 11. The mean ± standard deviation is presented. Statistical analysis was performed with Student’s t test (*p < 0.05; **p < 0.01; ***p < 0.001). C Analysis of NAMPT and NAPRT protein levels by Western blotting at Day 4, Day 7 and Day 11. D, E & F NAPRT as a resistance mechanism in NAMPT CRISPRs in HNSCC cell lines. D Clonogenic assay, E) clonal phenotype analysis. Analysis of the clone phenotypes (holoclones, meroclones and paraclones) formed by NAMPT CRISPRs and control cells in RPMI-2650 and Detroit-562 cell lines. In each solid bar, bottom part are holoclones, medium part are paraclones and upper part are meroclones. In Detroit, no meroclones were observed. F NAD quantification of NAMPT CRISPRs and (empty vector only, EV) cells under normal conditions (CONTROL) after nicotinic acid treatment (NA, 0.5 mM) and treatment with the NAPRT inhibitor 2-hydroxynicotinic acid (2HNA, 1 mM). 200 mg/kg 2HNA i.p. four times a week. G In vivo reduction of tumors by the NAMPT inhibitors GNE617 and GMX1778 in monotherapy and in combination with 2HNA (1 mM) in parental RPMI-2650 and Detroit-562 cell lines. All treatments lasted 3 weeks (gray band), and the tumor measurement was continued for two more weeks. In each cohort, N = 6. The mean ± standard deviation is presented. Statistical analysis was performed with Student’s t test (*p < 0.05; **p < 0.01; ***p < 0.001)

Back to article page