Development of various cancers [3]. Investigation of cancer-specific miRNAs and their targets is necessary for further elucidation of their role in the pathogenesis of tumors, and may be important for the design of novel therapeutic targets [6,8,17]. Although miRNAs have been widely studied in different types of cancers, the knowledge of the CEP-37440 cost aberrant expression and potential function of miRNAs in GC is largely lacking. Accumulating evidence shows that miR-107 is one of PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28298493 the oncogenic RNAs, and overexpression of these RNAs has been reported in several types of human malignantFigure 4 CDK8 was a direct target of miR-107. a: The relative luciferase activity (firefly/renilla) was measured in HEK293 cells after cotransfection of the CDK8 luciferase construct with either miR-107 mimics or NC. b: CDK8 mRNA level was detected by RT-PCR in SGC7901 cells transfected with miR-107 inhibitor or the control. c: CDK8 protein level was detected by Western blotting in SGC7901 cells transfected with miR-107 inhibitor or the control. *P < 0.05.solid tumors. Previously, Inoue et al. found that the mean expression level of miR-107 was significantly higher in the GC tissues compared to that of normal tissues. In theSong et al. Diagnostic Pathology 2014, 9:164 http://www.diagnosticpathology.org/content/9/1/Page 5 ofFigure 5 Down regulation of CDK8 attenuated the oncogenic effect of miR-107. *P < 0.05 compared with control. #P < 0.05 compared with miR-107 mimics group.software, then luciferase reporter vectors containing CDK8 gene 3-UTR region with miR-107 binding site was constructed and specific binding between miR-107 and CDK8 was verified. The expression level of CDK8 mRNA and protein in miR-107 inhibitor transfected GC cell line was significantly decreased compared with control group,, indicating that miR-107 suppressed CDK8 expression posttranscriptionally. CDK8 is a member of CDK family (CDKs), which is a group of serine-threonine protein kinase and consists of 10 members with different homology. In the past decade, It has been showed that CDKs were excessively activated in different tumors [20]. Preclinical studies have proved that CDKs can promote gene transcription, cell differentiation and angiogenesis [21]. In our study, MTT assay showed that down regulation of CDK8 by siRNA could significantly attenuate the oncogenic effect of miR-107, suggesting that miR-107 promoted the proliferation of GC cells partially by targeting CDK8.comparison of clinicopathological factors, miR-107 expression showed significant association with depth of tumor invasion, lymph node metastasis and tumor stage. In Kaplan-Meier survival curve analysis, OS and DFS of patients with high miR-107 expression were significantly worse than those of patients with low miR-107 expression. In the Cox multivariate analysis, it was shown that miR-107 expression in GC tissues was an independent prognostic factor for OS and DFS. Their results indicate that miR-107 may be useful as an effective biomarker for prediction of a poor prognosis in GC patients [13]. However, the detailed mechanisms of miR-107 were fewly investigated in GC. Previously, Feng et al. found that miR107 targeted cyclin-dependent kinase 6 (CDK6) expression, induced cell cycle G1 arrest and inhibited invasion in GC cells [18]. Li et al. found that upregulation of miR-107 induced proliferation in GC cells by targeting the transcription factor FOXO1 [19]. In the present study, we validated that the expression of miR-107 was s.