Thus, a deeper understanding of the molecular and genetic networks that control the initi ation and progression of CRC is imperative. MicroRNAs are small non coding RNAs that regulate gene expression by the inhibition of the translation and or decreasing of the stability of target mRNAs. MicroRNAs participate in gene regulation, apoptosis, hematopoietic selleck chem Ruxolitinib development, the maintenance of cell differentiation, and tumor genesis. Recent data suggest that dysregulation of miRNAs is an important step in the pathogenesis, from initiation to metastasis, of many cancers including CRC. The dysregulation of miRNA expression is associated with oncogenic transformation. MicroRNAs that act as tumor suppressors or oncogenes have been identified in many types of tumors. Strillacci et al.

reported an in verse correlation between COX 2 and miR 101 expression in colon Inhibitors,Modulators,Libraries cancer cell lines, and demonstrated the direct inhibition of COX 2 mRNA translation mediated by miR 101. Shen et al. found that miR 139 inhibits inva sion and metastasis Inhibitors,Modulators,Libraries of CRC by targeting the type I insulin like growth factor receptor. Recently, Sarver et al. using microarray analysis had shown that miR 32 was upregulated in CRC. In their study, the authors quantified the expression levels of 735 miRNAs in 80 human CRC samples and 28 normal colon tissues, and identified 39 miRNAs, including miR 32, whose expression levels were significantly altered in CRC samples. However, the func tion of miR 32 in CRC remains unknown. The phosphatase and tensin homologue pro tein is a well known anti oncogene.

PTEN is one of the most frequently mutated tumor suppressors in a variety of human cancers. Its loss of expression is asso ciated with tumor progression and poor clinical outcome in CRC. Nuclear Inhibitors,Modulators,Libraries PTEN expression gradually de creases during the Inhibitors,Modulators,Libraries normal adenoma adenocarcinoma se quence, which suggests an important role for PTEN in carcinogenesis. PTEN is a negative regulator of the PI3K Akt pathway, and the PTEN loss PI3K pAkt pathway may play an important role in sporadic colon carcinogenesis. Reduction of PTEN expression may pre dict relapse in CRC patients. Bioinformatics has shown that the 30 UTR of PTEN contains a putative bind ing site for miR 32. However, the regulation of miR Inhibitors,Modulators,Libraries 32 in CRC or it association with PTEN have not been reported. In this study, we focused on the expression and function of miR 32 in CRC cells. In gain of function and loss of function studies, we found that miR 32 promoted CRC cells growth, migration, invasion, and reduced apoptosis. Overexpression of miR 32 resulted in downregulation of PTEN at a posttranscriptional level. By using a luciferase reporter http://www.selleckchem.com/products/MDV3100.html gene, we identified PTEN as the functional down stream target of miR 32.