The signal transduction activities associated with mesenchymal cells that facilitate migration and survival in an anchorage-independent environment. The gain of mesenchymal cell markers such as Vimentin, Snail homolog 2, and fibronectin has been observed in tumor progression. In addition, cellular changes resulting in a more mesenchymal-like state are associated with poor prognosis. Mesenchymal-like tumor cells gain migratory capacity through abnormal survival signals via receptors such as fibroblast growth factor receptor, hepatocyte growth factor receptor, transforming growth factor beta receptors, insulin like growth factor 1 receptor, platelet derived growth factor receptor, and regulatory kinases such as phosphoinositide-3-kinase, v-akt murine thymoma viral oncogene, and mechanistic target of rapamycin. Nuclear factor of kappa light polypeptide gene enhancer in Bcells is upregulated in human breast tumor cell lines, carcinogen transformed mammary epithelial cells, the majority of primary human and rodent breast tumor tissue samples. It has been reported to be a central mediator of EMT in a mouse model of breast cancer progression. More recently, NF-kB was shown to act upstream of SNAI2 expression during EMT of MCF10A human mammary epithelial cells overexpressing a constitutively active IGF1R. SNAI2 can also repress endogenous E-cadherin gene expression. In breast cancer cell lines, SNAI2 levels were shown to correlate with loss of Ecadherin transport. Proteins of the tetraspanin family form complexes with integrins and function in cell-cell adhesion in a cadherin-independent manner. CD151 is the first of 33 tetraspanin family members associated with promotion of metastasis. In cancer cells, CD151 regulates adhesion-dependent signaling and post-adhesion events, including cell migration. CD151 also plays a role in the induction of EMT and the overall survival of patients with cancer. TGFb has been postulated to be a pro-oncogenic factor acting late in tumor progression. In transformed cells, TGFb enhances crucial metastatic processes, including the ability to degrade the extracellular matrix, cell invasiveness, and epithelial-mesenchymal transition. NF-kB and CD151 induction are required for the TGFb-mediated response. Here, we used enrichment analysis to identify miR-506 as being a miRNA that targets the 39 untranslated regions of EMTrelated genes such as SNAI2, VIM, and CD151. Importantly, we found an NF-kB binding motif upstream of the promoter region of miR-506. We therefore hypothesized that NF-kB binds upstream of the promoter region of miR-506, which further targets the 39UTR of CD151 and other EMT markers such as VIM and SNAI2 to regulate EMT. We previously investigated the function of miRNAs in tumor initiation, progression, and metastasis. In this study, we aimed to investigate the role of miRNAs in EMT. We therefore AbMole Diperodon considered genes related to the regulation of EMT from the Gene Ontology database and other independent studies. miRNAs predicted to target these genes were selected using TargetScan.