Second, in a tumor-bearing mouse model, a direct injection of miR-27a to tumor suppressed tumor growth. These findings strongly suggested that miR-27a could be used as a biomarker to monitor cancer development and progression, and could be used as a potential therapeutic target and even a potential therapeutic agent for coloSuramin sodium salt rectal cancer. The mechanistic studies further showed that miR-27a-mediated tumor suppressor could be through targeting SGPP1, Smad2 and STAT3. Previous studies have demonstrated that Apc mutation and Wnt/b-catenin signaling activation, and chronic inflammation in colon, are the two major causes for colorectal cancer formation. The studies from us have shown that genetic deletion of the Muc2 gene is sufficient to cause chronic colitis and rectal inflammation at early stage, and leads to colorectal cancer formation at late stage. The malignant transformation is Prochlorperazine dimaleate salt linked to the activation of inflammatory signaling and upregulation of cytokines. And the chronic inflammation facilitated Apc-mutation-caused gastrointestinal tumor formation in the Apc/Muc2 double gene knockout mouse model of colorectal cancer. In fact, other studies have demonstrated that the transcription factor STAT3 also plays a critical role in inflammation-associated colorectal cancer formation. During the transition of chronic intestinal inflammation to colitisassociated cancer, STAT3 could be persistently activated by sphingosine-1-phosphate produced by upregulation of sphingosine kinase 1, which was linked to production of the multifunctional NF-kB-regulated cytokine IL-6, and consequently upregulating of the S1P receptor, S1PR1. While, the balance of S1P levels are regulated by sphingosine-1-phosphate phosphatase 1. Using comprehensive approaches, including qRT-PCR, immublotting and in situ immunohistochemical staining, we showed that the expression of SGPP1 at mRNA and protein levels were upregulated in colorectal cancers and colorectal cancer cell lines, which were inversely correlated with the expression of miR-27a.Both dual luciferase assay and increasing expression of miR-27a further showed the inhibitory effects of miR-27a on SGPP1.