Background and Aims: Although the treatment of colorectal cancer has been increasingly improved, the current treatment efficacy remains unsatisfactory. Therefore, the consistent screening and identification of the critical molecules that play the regulatory roles in the initiation and progression of colorectal cancer along with revelation of their functions and actions is an important process to develop new diagnostic and therapeutic targets and eventually improve the treatment effect of colorectal cancer. Accordingly, this study was designated for the first time to investigate the expression level of carboxyl ester lipase (CEL) in colorectal cancer, and preliminarily analyze its biological function in colorectal cancer. 
Methods: Based on the UALCAN and GEPIA online databases containing cancer gene expression data, the expression of CEL and its promoter methylation status in colorectal cancer and normal tissues were analyzed. Then, the expression of CEL in colorectal cancer tissue/tumor adjacent normal tissue and colorectal cancer cell lines/normal human colonic epithelial cells were further determined by qPCR, immunohistochemical staining and Western blot, respectively. The expression level of CEL in human colorectal cancer SW620 cells was transiently knocked down by transfection with siRNA specifically targeting CEL (siCEL), after that, the primary biological functions of CEL in colorectal cancer were analyzed by CCK-8 assay, plate colony formation assay, Transwell migration and invasion assay, respectively. 
Results: The data from cancer-relevant databases showed that the expression of CEL in colorectal cancer tissues was significantly higher than that in normal tissues (P<0.05, P<0.001), and the promoter methylation level of CEL in colorectal cancer tissues was significantly lower than that in normal tissues (P<0.001). The results of qPCR, immunohistochemical staining and Western blot further confirmed that the gene and protein expression levels of CEL in colorectal cancer tissue were significantly higher than those in control tissue, and in colorectal cancer cells were significantly higher than those in normal colonic epithelial cells (P<0.01, P<0.001). In SW620 cells after CEL expression knock-down by siCEL transfection, the growth speed, colony?forming ability, as well as the migration and invasion abilities were all significantly inhibited (P<0.05, P<0.01, P<0.001). 
Conclusion: CEL expression is upregulated in colorectal cancer, which may be related to its hypomethylated promoter. The malignant biological behaviors of colorectal cancer cells can be inhibited by CEL knock-down, suggesting that high CEL expression promotes malignant progression of colorectal cancer. So, CEL may be a potential target for diagnosis and treatment of colorectal cancer.