Asporin has been implicated as an oncogene in various types of human cancers; 
however, the roles of asporin in the development and progression of colorectal 
cancer (CRC) have not yet been determined. With clinical samples, we found that 
asporin was highly expressed in CRC tissues compared to adjacent normal tissues 
and the asporin expression levels were significantly associated with lymph node 
metastasis status and TNM stage of the patients. Through knockdown of asporin in 
CRC cell lines RKO and SW620 or overexpression of asporin in cell lines HT-29 
and LoVo, we found that asporin could enhance wound healing, migration and 
invasion abilities of the CRC cells. Further more, with the human umbilical vein 
endothelial cells (HUVECs) tube formation assays and the xenograft model, we 
found that asporin promoted the tumor growth through stimulating the VEGF 
signaling pathway. The portal vein injection models suggested that asporin 
overexpression stimulated the liver metastasis of HT29 cell line, while asporin 
knockdown inhibited the liver metastasis of RKO cell line. In addition, asporin 
was found to augment the phosphorylation of EGFR/src/cortactin signaling 
pathway, which might be contributed to the biological functions of asporin in 
CRC metastasis. These results suggested that asporin promoted the tumor growth 
and metastasis of CRC, and it could be a potential therapeutic target for CRC 
patients in future.