关键词: CHIP E-ca E-cadherin EMT FBS FN HBV HCC HNSCC Hepatitis B virus Hepatocellular carcinoma Invasion KLF-17 KLF17 Krüppel-like factor 17 MT Vim WT chromatin immunoprecipitation epithelial mesenchymal transition fetal calf serum fibronectin head and neck squamous cell carcinoma hepatocellular carcinoma microRNA-9 mutant type qRT-PCR quantitative reverse transcription polymerase chain reaction vimentin wild type

Mesh : Blotting, Western Carcinoma, Hepatocellular / genetics metabolism Cell Line, Tumor Cell Movement / genetics physiology Chromatin Immunoprecipitation Humans Liver Neoplasms / genetics MicroRNAs / genetics metabolism Protein Binding Reverse Transcriptase Polymerase Chain Reaction Transcription Factors / genetics metabolism

来  源:   DOI:10.1016/j.molonc.2013.04.007   PDF(Sci-hub)

Abstract:
Metastasis is one of the hallmarks of cancer malignancy that usually causes more detrimental effects than a primary tumor. Many microRNAs were reported to be involved in the process of tumor metastasis. Hep11 and Hep12 cells were derived from primary and recurrence (intrahepatic metastatic) sites of hepatocellular carcinoma (HCC), respectively. Hep12 exhibited a higher invasive and migratory potential than Hep11. There was also a significantly higher expression of miR-9 in Hep12 cells than in Hep11 cells. Further studies in HCC cell lines demonstrated that miR-9 could promote tumor cell migration and invasion. In addition, miR-9 downregulated KLF17 protein expression by targeting the 3\'UTR region of the KLF17 gene directly. As a transcription factor, KLF17 directly acted on the promoters of EMT-related genes (ZO-1, Vimentin and Fibronectin (FN)) in HCC cell lines. Therefore, we conclude that miR-9 may possibly promote HCC migration and invasion through regulation of KLF17.
摘要:
转移是癌症恶性肿瘤的标志之一,通常比原发性肿瘤引起更有害的影响。据报道,许多microRNA参与了肿瘤的转移过程。Hep11和Hep12细胞来自肝细胞癌(HCC)的原发和复发(肝内转移)部位,分别。Hep12表现出比Hep11更高的侵入性和迁移潜力。miR-9在Hep12细胞中的表达也显著高于Hep11细胞。在HCC细胞系中的进一步研究表明,miR-9可以促进肿瘤细胞的迁移和侵袭。此外,miR-9通过直接靶向KLF17基因的3'UTR区下调KLF17蛋白表达。作为转录因子,KLF17直接作用于HCC细胞系中EMT相关基因(ZO-1,波形蛋白和纤连蛋白(FN))的启动子。因此,我们得出结论,miR-9可能通过调节KLF17促进HCC的迁移和侵袭。
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