ArticleInternational journal of molecular sciences2015
Epigenetic Repression of miR-218 Promotes Esophageal Carcinogenesis by Targeting ROBO1.
Article in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Cigarette Smoke Enhances the Malignant Phenotype of Esophageal Adenocarcinoma Cells by Disrupting a Repressive Regulatory Interaction Between miR-145 and LOXL2.Laboratory investigation; a journal of technical methods and pathology · 2023Article
- PES1 reduces CD8Journal of biomedical science · 2023Article
- Role of gene signature regulation in tumor immune microenvironment on the mechanism of uveal melanoma metastasis.Cancer biomarkers : section A of Disease markers · 2023Article
- Roles of microRNAs in tumorigenesis and metastasis of esophageal squamous cell carcinoma.World journal of clinical oncology · 2021Review
- LncRNA SNHG10 increases the methylation of miR-218 gene to promote glucose uptake and cell proliferation in osteosarcoma.Journal of orthopaedic surgery and research · 2020Article
- miR‑218 functions as a tumor suppressor gene in cervical cancer.Molecular medicine reports · 2020Article
- The Role of the Slit/Robo Signaling Pathway.Journal of Cancer · 2019Review
- [MicroRNA-218 promotes osteosarcoma cell apoptosis by down-regulating oncogene B lymphoma mouse Moloney leukemia virus insertion region 1].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2018Article
- lncRNA HOTAIR Contributes to 5FU Resistance through Suppressing miR-218 and Activating NF-κB/TS Signaling in Colorectal Cancer.Molecular therapy. Nucleic acids · 2017Article
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8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
miR-218, consisting of miR-218-1 at 4p15.31 and miR-218-2 at 5q35.1, was significantly decreased in esophageal squamous cell carcinoma (ESCC) in our previous study. The aim of this study was to determine whether aberrant methylation is associated with miR-218 repression. Bisulfite sequencing analysis (BSP), methylation specific PCR (MSP), and 5-aza-2'-deoxycytidine treatment assay were applied to determine the methyaltion status of miR-218 in cells and clinical samples. In vitro assays were performed to explore the role of miR-218. Results showed that miR-218-1 was significantly CpG hypermethylated in tumor tissues (81%, 34/42) compared with paired non-tumor tissues (33%, 14/42) (p < 0.05). However, no statistical difference was found in miR-218-2. Accordingly, expression of miR-218 was negatively correlated with miR-218-1 methylation status (p < 0.05). After demethylation treatment by 5-aza-2'-deoxycytidine, there was a 2.53- and 2.40-fold increase of miR-218 expression in EC109 and EC9706, respectively. miR-218 suppressed cell proliferation and arrested cells at G1 phase by targeting 3' untranslated region (3'UTR) of roundabout guidance receptor 1 (ROBO1). A negative correlation was found between miR-218 and ROBO1 mRNA expression in clinical samples. In conclusion, our results support that aberrant CpG hypermethylation at least partly accounts for miR-218 silencing in ESCC, which impairs its tumor-suppressive function.
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