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Tumor-suppressive miR-3650 inhibits tumor metastasis by directly targeting NFASC in hepatocellular carcinoma

机译:肿瘤抑制miR-3650通过直接靶向NFASC抑制肝细胞癌的肿瘤转移

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摘要

In recent years, a growing body of evidence has provided support for the important role of microRNAs (miRNAs) in the progression of human cancers. A recent study showed that a novel miRNA miR-3650 expression was significantly decreased in hepatocellular carcinoma (HCC). However, the precise role of miR-3650 in HCC have remained poorly understood. In this study, we found that miR-3650 expression was frequently decreased in HCC tissues. Low expression of miR-3650 is positively associated with tumor metastasis and poor survival of HCC patients. Forced expression of miR-3650 significantly inhibited the migration and epithelial-mesenchymal transition (EMT) of HCC cells. Through bioinformatic analysis and luciferase assays, we confirmed that neurofascin (NFASC) is a directly target mRNA of miR-3650. Rescue experiment demonstrated that NAFSC overexpression could partially counteracted the inhibitory effect of miR-3650 in HCC metastasis and EMT. In conclusion, our findings are the first time to demonstrate that reduced expression of miR-3650 in HCC was correlated with tumor metastasis and poor survival. MiR-3650 repressed HCC migration and EMT by directly targeting NFASC. Our findings suggested that miR-3650 may serve as a potential prognostic marker and promising application in HCC therapy.
机译:近年来,越来越多的证据为microRNA(miRNA)在人类癌症进展中的重要作用提供了支持。最近的一项研究表明,在肝细胞癌(HCC)中,新型miRNA miR-3650的表达明显降低。但是,人们对miR-3650在肝癌中的确切作用仍知之甚少。在这项研究中,我们发现miR-3650在肝癌组织中的表达经常降低。 miR-3650的低表达与HCC患者的肿瘤转移和较差的生存呈正相关。强迫表达的miR-3650可显着抑制HCC细胞的迁移和上皮-间质转化(EMT)。通过生物信息学分析和萤光素酶测定,我们证实了神经法索霉素(NFASC)是miR-3650的直接靶mRNA。救援实验表明,NAFSC的过表达可以部分抵消miR-3650对HCC转移和EMT的抑制作用。总之,我们的发现是首次证明miR-3650在肝癌组织中的表达减少与肿瘤转移和不良生存率相关。 MiR-3650通过直接靶向NFASC抑制了HCC迁移和EMT。我们的发现表明,miR-3650可能是潜在的预后标志物,并有望在HCC治疗中应用。

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