Fig. 2

Dexamethasone (DEX), forskolin (FSK) and heat shock treatments reduce B16 cell proliferation. a, b Representative flow cytometry dot plots and c–e overall analysis for cell cycle phases in B16 cells 24–44 h after DEX treatment (or untreated), stained for incorporated BrdU and with 7AAD. Significant rhythms are illustrated with fitted cosine curves, otherwise data are connected by straight lines between data points, indicating no significant circadian rhythms (n = 24, 6 wells/time point, cosine-wave regression, F-test: Control: all genes/phases p > 0.05, DEX: p < 0.05; two-way ANOVA, posthoc test, group: **p < 0.01, ***p < 0.001). f, g Total alive cell numbers 12–48 h (f) and 48–68 h (g) after treatment with either DEX or FSK and controls (n = 6–8 wells/time point). h Alive cell numbers 0–96 h after control or DEX treatment at 0 h (1x DEX) or at 0 and 48 h (2x DEX) (n = 4–12 wells/time point). i Alive cell numbers 0–72 h after heat shock or control treatment (n = 6 wells/time point). Two-way ANOVA, posthoc test, *p < 0.05, **p < 0.01, ***p < 0.001 for DEX compared to controls; ⁺⁺⁺ p < 0.001 FSK compared to controls; ^## p < 0.01 compared to 1x DEX; ^x p < 0.05, ^xx p < 0.01, ^xxx p < 0.001 compared to 2x DEX. Data are represented as mean ± standard error of the mean. For details of statistics, see Additional file 1