Hepatocellular carcinoma (HCC) is a primary cause of cancer-related mortality worldwide [1]. Currently, HCC is second in incidence among the various tumors in Egyptian men, and its burden is expected to increase due to the high predominance of chronic viral hepatitis C (HCV) infection [2]. The majority of patients with HCC is diagnosed at late stages and usually has inoperable tumors, and thus receives palliative treatments [3]. Moreover, a large portion of HCC cells have a tendency to metastasize to different organs including lungs, lymph nodes and bones, which results in poor prognosis of patients [4]. Therefore, understanding the molecular pathways that are involved in the progression of the disease is important for the development of novel therapeutics.

Epithelial-mesenchymal transition (EMT) has been reported to be an important mechanism contributing to cancer invasion and metastasis in epithelial-derived cancer types, including HCC [5]. The characteristic changes that occur during EMT include the downregulation of epithelial markers, such as E-cadherin [6], and the upregulation of mesenchymal markers, including vimentin [6]. E-cadherin is a trans-membrane glycoprotein that forms the core of the adherent junctions between adjacent epithelial cells. E-cadherin is involved in regulating cell–cell adhesions, mobility and proliferation of epithelial cells, and has a potent invasive suppressor role [7]. The expression of E-cadherin is regulated by various transcription factors, including Snail, Slug, Twist, ZEB1 and ZEB2. These transcription factors able to bind the E-box sequence in the promoter region of E-cadherin, controlling its expression [8].

MicroRNAs (miRNAs/miRs) are a well-known group of small non-coding RNAs that are involved in post-transcriptional gene regulation in diverse biological processes, including cell proliferation, apoptosis and cell cycle. In addition, miRNAs function as both tumor suppressors and promoters in numerous aspects of the autonomous features of cancer cells [9]. Several miRNAs are important regulators of the expression of EMT-activating signaling pathways related genes via controlling E-cadherin expression in cancer cells [10]. Previous studies reported that miR-200 is mainly involved in regulating the epithelial characteristics of cells by suppressing ZEB family [11], [12]. It has also been shown that silencing of miR-200 family member can induce EMT and invasion in epithelial cancer cells, which suggests the involvement of miRNAs in progression and metastasis of HCC [13]. Therefore, understanding the role of miRNAs in controlling the EMT pathway in HCC may reveal novel markers and targets in HCC management. Thus, the aim of the present study was to investigate the involvement of miRNAs in the progression of HCC in fresh tissues collected from newly diagnosed Egyptian patients.