The majority of human cancers originate from epithelial cells [1], with their local invasion and metastasis accounting for 90% of cancer-related death [2]. The progression of metastasis is a complex event thought to incorporate the reversible developmental process of epithelial to mesenchymal transition (EMT). This involves cancerous epithelial cells transitioning into motile mesenchymal cells, which invade distant sites in the body where they lodge and undergo mesenchymal to epithelial transition (MET) before proliferating into secondary tumours [3]. Essential to the maintenance of the polarised epithelial monolayer is the adherens junction protein, E-cadherin, which has been described as a tumour suppressor because its down-regulation is associated with invasion and metastasis [4]. During EMT, the increase of transcription factors, such as ZEB1, SIP1, Snail, and Slug, strongly represses the transcription of the E-cadherin gene, facilitating loss of the strong cell-cell interactions characteristic of epithelial cells. First discovered in 1993, microRNAs (miRNAs) are an abundant class of noncoding, 18–25 nt, single-stranded oligoribonucleotides that function post-transcriptionally to negatively regulate the translation of messenger RNA (mRNA). Target recognition is based on complementary binding to the 3’untranslated region (3’UTR) of the target mRNA. Expression of miRNAs can vary from ubiquitous to highly site and/or temporal specific. They are predicted to regulate up to 30% of genes in eukaryotes [5] and have regulatory roles in cellular processes, such as proliferation [6, 7, 8], differentiation [9], apoptosis [10, 11], metabolism [12], embryogenesis and developmental timing [13, 14, 15, 16]. Consistent with their roles in maintaining normal cell function, the aberrant expression of miRNAs has been linked to oncogenesis [17] and, more recently, metastasis [18, 19, 20, 21, 22]. Since EMT is an essential developmental process and is implicated in metastasis, we postulated that miRNAs may be involved in its regulation.

Evidence that EMT is required for cancer metastasis is increasing with investigations into the signalling mechanisms driving EMT. A potent inducer of EMT is the cytokine transforming growth factor-β (TGF-β), which has been implicated in regulating transcription factors including Snail, Slug, ZEB1, SIP1, and basic-helix-loop-helix (bHLH) factors, such as Twist [23, 24]. However, knowledge of the role of miRNAs and their potential target genes in EMT is limited. Previous studies have shown that