Crosstalk between miR-215 and epithelial-mesenchymal transition specific markers (E-cadherin and N-cadherin) in different stages of chronic HCV Infection.

Abstract

The main causes of death among patients with hepatocellular carcinoma (HCC) are a recurrence, metastasis, and deterioration of primary tumors by the epithelial-to-mesenchymal transition (EMT) which is controlled by several molecules including E-cadherin and N-cadherin. Microribonucleic acids (miRNAs) have been identified to play a regulatory role in EMT. miR-215 is important in repressing migration/invasion of cancer cells. In this study, we aimed to evaluate the crosstalk between miR-215 and EMT specific markers (E-cadherin and N-cadherin) with a spotlight on its role in the EMT process in hepatitis C virus (HCV)-infected patients. One hundred forty-five patients were studied, 75 had HCV-induced cirrhosis classified into child A, B, and C and 25 had HCC. In parallel, 45 healthy volunteers considered as controls. Serum levels of E- and N-cadherin were measured using enzyme-linked immunosorbent assay and miR-215 expression measured by a quantitative reverse transcription-polymerase chain reaction. Insignificant change in serum levels of E-cadherin and N-cadherin in HCV-infected patients compared with normal controls was observed with a slight increase in E-cadherin and N-cadherin in the child B group. HCC patients had the lowest amount of E-cadherin and N-cadherin compared with cirrhotic and normal subjects. A maximum reduction in miR-215 was observed in HCC patients compared with cirrhotic and control ones. A positive correlation (r = .202; P < .05) was observed between miR-215 and E-cadherin. Our data stressed on the potential role of miR-215 as an important mediator in HCC progression. miRNAs participating in EMT needs further studies to provide insight into the metastasis of HCC.