Abstract The traditional Chinese medicine, “Hong-Qu”, also call “red mold rice” in the United States and Europe, has been identified and used for the treatment of blood stasis, a disorder related to hyperlipidemia and atherosclerosis. In addition to its value in improving metabolism syndrome, extracts from Monascus fermented rice inhibited proliferation of various cancer cells in vitro and in vivo have demonstrated previously. The objective of the current study was to examine correlation of red mold rice ethanol extract (RMRE) on the process of angiogenesis, invasion and metastasis during tumor progression. In the current study, we examined the inhibitory effects of SW480 and SW620 human colorectal carcinoma cells by RMRE using in vitro MTT assay. RMRE significantly inhibited the proliferation of SW480 and SW620 cells in dose- and time-dependent manner. However, human umbilical vein endothelial cells (HUVECs) showed a minor reduction effect of cell viability up to 20 µg/mL of RMRE for 48 hours using crystal violet staining assay. The capillary-like network morphology was observed following 20 ng/mL VEGF or SW620 culture-conditional medium (CM) addition. Nevertheless, capillary-like tube formation have failed to show when RMRE participation. Moreover, SW620 cells could growth in Matrigel grafts and spontaneously intravasation from the upper to the lower of chick embryo chorioallantoic membrane (CAM) model, which detected human Alu genomic DNA by PCR amplification from the lower CAMs at RMRE-untreated group. The percentage of neovascularization was increased 75.3±11.6% by SW620 cells onplant with Matrigel grafts on the CAM model. However, addition of RMRE significantly reduced CAM neovascularization in dose-dependent effect. Finally, we have finding that RMRE effectively decreased activity of matrix metalloproteinase (MMP)-7 determined by RT-PCR, Western blotting, and casein zymography assays. In summary Monascus fermented products exerted a potent effect on tumor growth and activation, suggesting that it may useful serves as a supplementary agent in adjuvant cancer therapy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 467.