Several studies have also observed that miR-27a exhibited oncogenic activity by directly suppressing ZBTB10/RINZF expression, resulting in upregulation of transcription factor specificity protein, vascular endothelial growth factor and VEGF receptor 1. In another hand, miR27a has also shown tumor suppressor roles, such as miR-27a is downregulated in esophageal cancers, oral squamous cell carcinoma, acute leukemia, and in non-small cell lung cancer. In NSCLC, miR-27a directly targets MET and EGFR 39 UTR, leading to reduced expression of MET and EGFR. This study was to determine the expression of miR-27a and association with colorectal Sertindole cancer formation, progression and the underlying mechanisms. We found that miR-27a was significantly reduced in human colorectal cancer tissues and in colorectal cancer cell lines. Using the approaches of miRNA array, systemic biology, in vitro manipulating expression of miR-27a and in vivo tumor-bearing mouse model, we found that miR-27a acted as a tumor suppressor in colorectal cancer, which was through targeting SGPP1 and Smad2. It is well known that the functions and target genes of a miRNA are tissue- and cancer-type specific. Functional studies have shown that miR-27a has shown both oncogenic and tumor suppressive functions in different cell lines and human cancer tissues. For example, miR-27a directly suppresses ZBTB10/RINZF expression. and in turn upregulates VEGF and VEGF receptor in the cancers of breast and colon, and overexpression of miR-27a is associated with poor outcomes. Whereas, in the cancers of esophagus, oral cavity, lung, and head and neck, miR-27a is downregulated, and miR-27a directly targets MET and EGFR and suppresses their expression in lung cancer. In this study, we found that miR-27a was significantly downregulated in colorectal cancers and colorectal cancer cells. Importantly, the downregulated miR-27a was also associated with colorectal cancer pathological stages and distant metastasis, showing tumor suppressor roles in colorectal cancer.First, in vitro studies showed that Nitisinone increased expression of miR-27a inhibited colorectal cancer cell proliferation, promoted apoptosis and attenuated cancer cell migration.