Xylopine Induces Oxidative Stress and Causes G₂/M Phase Arrest, Triggering Caspase-Mediated Apoptosis by p53-Independent Pathway in HCT116 Cells

Table 3

Effect of xylopine (XYL) in the cell cycle distribution of HCT116 cells.

Treatment	Concentration (μM)	DNA content (%)
		Sub-G0/G1	G0/G1	S	G2/M
24 h incubation
CTL	—	3.9 ± 1.0	42.0 ± 2.5	12.6 ± 2.8	30.7 ± 4.1
DOX	1	9.7 ± 2.5	28.0 ± 6.3	10.0 ± 2.5	44.1 ± 3.4
OXA	2.5	8.8 ± 3.5	32.4 ± 3.7	13.5 ± 3.1	39.9 ± 1.5
XYL	3.5	6.2 ± 1.9	17.0 ± 7.0	24.7 ± 4.8	57.2 ± 3.5
	7	5.1 ± 1.6	14.9 ± 4.2	23.3 ± 3.7	58.5 ± 2.9
	14	11.3 ± 1.4	30.5 ± 6.0	11.1 ± 1.6	54.0 ± 6.1
48 h incubation
CTL	—	3.3 ± 0.7	44.8 ± 1.1	13.5 ± 2.4	23.8 ± 2.8
DOX	1	18.3 ± 2.5	22.5 ± 4.0	14.9 ± 2.5	44.2 ± 4.4
OXA	2.5	17.7 ± 1.9	36.2 ± 2.6	7.6 ± 0.4	32.2 ± 4.4
XYL	3.5	15.2 ± 1.9	17.0 ± 6.3	11.1 ± 2.2	52.0 ± 6.8
	7	25.9 ± 2.5	10.3 ± 1.3	6.8 ± 2.0	52.7 ± 3.6
	14	33.4 ± 6.2	14.6 ± 2.6	9.3 ± 1.7	40.8 ± 5.7

Data are presented as the mean ± S.E.M. of three independent experiments performed in duplicate. The negative control (CTL) was treated with the vehicle (0.1% DMSO) used for diluting the compound tested. Doxorubicin (DOX) and oxaliplatin (OXA) were used as positive controls. Ten thousand events were evaluated per experiment, and cellular debris was omitted from the analysis. compared with the negative control by ANOVA followed by Student–Newman–Keuls test.