However, the functional significance of increased Ifna1 in transformed IEC-6 cells was unclear. Cdh1 was showed to be AZD2014 mouse down regulated in transformed IEC-6 cells, which was coincident with others’ findings. Cdh1 played a key role in cell-cell adhesion. Inactivation of the cdh1 mediated cell adhesion system was a common finding in human cancers, indicating that cdh1 function as tumor suppressor and Foretinib invasion suppressor genes [29, 30]. miRCURY microRNA chips contained totally 2056 probes, including human, mouse and rat miRNA genes. So it has been broadly applied in many research works [31, 32]. Our data indicated several miRNAs were highly expressed

in IEC-6 cells and 20 miRNAs showed evidence of being differentially expressed within

the transformed IEC-6 cells. Among these differentially expressed miRNAs, we verified the alteration of miR-208 and miR-22*. miR-208 is encoded by intron 27 of the human and mouse MHC gene. Consistent with the specific expression of MHC in the heart and the pulmonary myocardium, miR-208 is expressed specifically in the heart and at trace levels in the lung [33]. The relationship between miR-208 check details and tumorigenesis was not clear and needed further study. miR-22* and miR-22 are the alternative mature type of their primary precursors. Increased miR-22 was found in erythropoiesis, and it was predicted to target genes involved in cell development and differentiation [34]. Our http://www.selleck.co.jp/products/Metformin-hydrochloride(Glucophage).html result showed miR-22* was increased, but not miR-22. This suggested that the maturation of primary precursor was selectively processed. Partial differential expressed miRNAs in transformed IEC-6 cells were consistent with the results of others.

Gottardo F et al found significant up-regulation of miR-185 in renal cell carcinoma compared to normal kidney [35]. Many targets have been reported for miR-185, including genes of the proto-cadherin gene cluster. However, we didn’t find the directly relationship between altered miRNAs and the specific genes in our experiment. Our results suggested that transformation of IEC-6 cells did not derived from a single gene, but rather through accumulated changes in the expression of several different genes involved in many biological pathways. So it was necessary to find out the reason why genes were deregulated at chromosomal levels. In the past few decades, evidence has accumulated showing that modifications of histone acetylation status have a central role in carcinogenesis [36–38]. Aberrant activation of histone deacetylases in tumour cells leads to transcriptional deregulation of a diverse set of genes mainly involved in the regulation of proliferation, migration, angiogenesis, and invasion. In this study, we showed that the increased level of acetylation of histone H3 was observed in transformed IEC-6 cells.