Research Advances in Antitumor Mechanism of Evodiamine

Table 4

Inhibition of microangiogenesis and migration by evodiamine in cancer cell lines in vitro or in vivo.

Cell line	Cell type/animal models	Specific results	Mode of action	References
HepG2, SMMC-7721, H22	Hepatocellular carcinoma BALB/c nude mice	(1) To evaluate the effect of evodiamine on VEGF-induced angiogenesis, Matrigel plug assays were performed with C57BL/6 mice. The addition of evodiamine (200 μg) to the plugs containing VEGF inhibited vascular formation. These plugs displayed a paler appearance, and fewer blood vessels were observed.; (2) HepG2 cells and SMMC-7721 cells were exposed to 0, 5, 10, or 20 μmol/L of evodiamine for 24 h. Representative images of cell migration and invasion were assessed with Transwells.	Inhibiting β-catenin and reducing VEGFa expression	[74]
PC-3 and DU145	Prostate cancer	PC-3 and DU145 cells were treated with 5 µM evodiamine for 24, 36, and 48 h. Evodiamine substantially downregulated the expression of VEGF.	Inhibiting the c-Met/Src/STAT3 signaling pathway	[75]
HT-29 and HCT-116	Colorectal cancer BALB/c nude mice	After treatment with different concentrations of evodiamine (0 or 1.5 μmol/L) for 24 h, the migration rates were detected. Wound-healing assay showed that treatment with evodiamine (1.5 μmol/L) significantly repressed the migration of HT-29 cells and HCT-116 cells.	Activating Sirt1	[76]
HCT-116	Colorectal cancer	Migration potential was assessed by Transwell assay after the cells had been treated by agents. The cells were seeded in the upper well of a Transwell insert, incubated with 10 µg/mL PGI/AMF and with 10 µg/mL PGI/AMF +6 µmol/L evodiamine for 28 h. Normal cells served as the control group. Evodiamine significantly inhibited PGI-induced migration in HCT-116 cells.	Inactivating the JAK2/STAT3 pathway through the downregulation of PGI	[77]