Research Advances in Antitumor Mechanism of Evodiamine

Table 2

Induction of cell cycle arrest by evodiamine in cancer cell lines in vitro.

Cell line	Cell type	Specific results	Mode of action	References
U2OS	Osteosarcoma	Evodiamine treatment at a range of concentrations (0, 3, 6, and 12 μM) triggered G2/M cell cycle arrest (9%–77%) for 24 h.	Inhibiting the Raf/MEK/ERK signaling pathway	[46]
A549	Lung cancer	Evodiamine treatment at a range of concentrations (0, 1, 2, and 4 μM) triggered G2/M cell cycle arrest (15.8%–86.2%) for 24 h.	Downregulation of ERK	[47]
COLO205 and HT-29	Colorectal carcinoma	Evodiamine treatment at a range of concentrations (0, 1, 2, and 4 μM) triggered G2/M cell cycle arrest for 24 h; evodiamine treatment at 2 μM triggered G2/M cell cycle arrest for 6, 12, and 24 h.	JNK activation	[48]
MDA-MB-231	Breast cancer	Exposure to different concentrations of evodiamine (0, 15, 30, 60, 90, and 120 µM) caused G0/G1 arrest of MDA-MB-231 (53.29%–60.12%) for 24 h.	Decreasing Bcl-2, cyclin D1, and cyclin-dependent kinase 6 expression	[49]
MCF-7 and MDA-MB-231	Breast cancer	Cell cycle analyses in monolayer culture (condition with FBS, without FBS), sphere culture condition. Evodiamine (0, 100, and 200 nM) mildly but significantly increased the proportion of cells at the G1 stage.	Activating the p53-p21-Rb pathway	[50]