Content area
Full Text
Received Jan 16, 2018; Accepted Mar 19, 2018
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
1. Introduction
Hepatocellular carcinoma (HCC) is one of the most common causes of cancer-related deaths worldwide, with high incidence of tumor recurrence and metastasis [1]. Identification of molecular markers plays a critical role in predicting the clinical outcome and promoting individual therapies for patients with HCC [2, 3].
MicroRNAs (miRNAs) have been implicated in regulation of pathogenesis of human tumors and could be potential biomarkers for diagnosis and prognosis [4, 5]. Recent studies have demonstrated that miRNAs participate in diverse human cancers processes including cell differentiation, proliferation, and apoptosis, as well as invasion and metastasis. For instance, miR-125 is a tumor suppressor that can decrease cell proliferation and metastasis through suppressing LIN28B expression in HCC [6], while miR-122a exerts tumor promoting effects on HCC by p53-dependent way [7]. Thus, cancer-specific miRNAs might be promising targets for cancer therapy [8].
Recently, miRNAs are demonstrated to function as critical regulators of cancer invasion and metastasis [9]. In our previous work, miR-219-5p is identified as one of the significant metastasis-related miRNAs in HCC [10]. However, little is known of the possible mechanism of miR-219-5p involved in HCC metastasis. In the present study, we found that miR-219-5p was upregulated in HCC tissues, was related to overall survival (OS) time of HCC patients, and promoted the proliferation and metastasis of HCC cells via downregulating CDH1. These results provide a clear understanding of the underlying mechanism by which miR-219-5p promotes HCC metastasis.
2. Materials and Methods
2.1. Clinical Tissue and Cell Culture
HCC tissues were obtained from patients who are treated with surgical resection in Huashan Hospital, Fudan University, and each patient had specific clinical-pathological information. Before surgical operations and collections of clinical tissues, all individuals wrote informed consent.
Human HCC cell lines Hep3B, Huh7, HepG2, MHCC-97H, and HCCLM3 were cultured in DMEM (Gibco) with 10% FBS. And they were propagated at 37°C in 5% CO2.
2.2. Cell Transfection
HepG2 and MHCC-97H cells were transfected with miR-219-5p mimic (50 nM) and miR-219-5p antagomir (400 pmol/ml) according to the manufacturer instructions. miR-219-5p mimic, antagomir,...