Most solid tumors are derived from epithelial tissues. The epithelial cells are highly polarized and hold together by junction proteins. During tumorigenesis, multiple steps are required to transform epithelia into tumor cells. The molecular mechanism of cell migration/ invasion is extensive studied in the culture cells. However, it is difficult to trace the process of tumorigenesis in vivo. Drosophila wing disc is a monolayer epithelium and pattern formation of wing discs is well studied. miRNAs are endogenous noncoding RNA. Mature miRNAs are 21-22 nucleotides and negatively regulate gene expression at posttranscriptional level. Several miRNAs function as oncogenes. In this study, we use Drosophila wing epithelia as a model to establish a system to study whether miRNAs induce tumorigenesis and promote the epithelial cells into invasive cells. To explore whether expression of miRNAs promotes epithelial cells into invasive cells, we use the GAL4/UAS system to express miRNAs in developing wing cells. dpp-GAL4 is expressed in the anterior/posterior boundary. We expressed UAS-miRNA and UAS-GFP by the dpp-GAL4 driver. The GFP reporter marks the miRNA expression cells. If the miRNAs promote epithelial cell invasion, the GFP expression cells will move from anterior/posterior boundary to the lateral regions. One hundred and fifty UAS-miRNA lines were screened. Preliminary, we isolated several microRNAs, mir-8, mir-274, mir-310, mir-318 and mir-1000 which can induce cell migration/invasion in wing epithelial cells. We further examine the epithelial and mesenchymal markers and possible downstream signalings induced by microRNAs. In this study, we established a novel system to study the function of microRNAs on cell invasion in Drosophila wing epithelial cells. This system will be useful to study the roles of microRNAs and their human homolog on tumor metastasis.