ArticleLaboratory investigation; a journal of technical methods and pathology2018
miR-137 is a tumor suppressor in endometrial cancer and is repressed by DNA hypermethylation.
Article in Laboratory investigation; a journal of technical methods and pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Identification of common salivary miRNA in oral lichen planus and oral squamous cell carcinoma: systematic review and meta-analysis.BMC oral health · 2024Pooled it
- Epigenetic silencing of miR-141 via core promoter methylation is associated with short-term bladder cancer progression.The Journal of biological chemistry · 2026Article
- From Epigenetic Dysregulation to Therapeutic Reprogramming in Endometrial Cancer: A State-Response Framework for Treatment Resistance.International journal of molecular sciences · 2026Review
- Molecular Links Between Smoking, COPD, and Lung Cancer: A DNA Methylation Perspective.Cancers · 2026Article
- Building a Hand-Curated ceRNET for Endometrial Cancer, Striving for Clinical as Well as Medicolegal Soundness: A Systematic Review.Non-coding RNA · 2025Review
- Advances in MiRNAs Involved in Endometrial Carcinoma.Combinatorial chemistry & high throughput screening · 2025Review
- miR-137: a potential therapeutic target for lung cancer.Frontiers in cell and developmental biology · 2024Review
- A feedback loop between lncRNA MALAT1 and DNMT1 promotes triple-negative breast cancer stemness and tumorigenesis.Cancer biology & therapy · 2023Article
- PDIA6, which is regulated by TRPM2-AS/miR-424-5p axis, promotes endometrial cancer progression via TGF-beta pathway.Cell death & disease · 2023Article
- Oral squamous cell carcinomas: state of the field and emerging directions.International journal of oral science · 2023Review
- Review
- The interplay of sex steroid hormones and microRNAs in endometrial cancer: current understanding and future directions.Frontiers in endocrinology · 2023Review
- Mitochondrial Genetic and Epigenetic Regulations in Cancer: Therapeutic Potential.International journal of molecular sciences · 2022Review
- Prognostic Value of miR-137 in Children with Medulloblastoma and its Regulatory Effect on Tumor Progression.Neuromolecular medicine · 2022Article
- Article
- Functional Screen for microRNAs Suppressing Anchorage-Independent Growth in Human Cervical Cancer Cells.International journal of molecular sciences · 2022Article
- The long and short non-coding RNAs modulating EZH2 signaling in cancer.Journal of hematology & oncology · 2022Review
- Article
- MiR-137-mediated negative relationship between LGR4 and RANKL modulated osteogenic differentiation of human adipose-derived mesenchymal stem cells.Genetics and molecular biology · 2022Article
- Epi-miRNAs: Regulators of the Histone Modification Machinery in Human Cancer.Journal of oncology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Endometrial cancer is the most common gynecological cancer in the United States. We wanted to identify epigenetic aberrations involving microRNAs (miRNAs), whose genes become hypermethylated in endometrial primary tumors. By integrating known miRNA sequences from the miRNA database (miRBase) with DNA methylation data from methyl-CpG-capture sequencing, we identified 111 differentially methylated regions (DMRs) associated with CpG islands (CGIs) and miRNAs. Among them, 22 DMRs related to 29 miRNAs and within 8 kb of CGIs were hypermethylated in endometrial tumors but not in normal endometrium. miR-137 was further validated in additional endometrial primary tumors. Hypermethylation of miR-137 was found in both endometrioid and serous endometrial cancer (P < 0.01), and it led to the loss of miR-137 expression. Treating hypermethylated endometrial cancer cells with epigenetic inhibitors reactivated miR-137. Moreover, genetic overexpression of miR-137 suppressed cancer cell proliferation and colony formation in vitro. When transfected cancer cells were implanted into nude mice, the cells that overexpressed miR-137 grew more slowly and formed smaller tumors (P < 0.05) than vector transfectants. Histologically, xenograft tumors from cancer cells expressing miR-137 were less proliferative (P < 0.05), partly due to inhibition of EZH2 and LSD1 expression (P < 0.01) in both the transfected cancer cells and tumors. Reporter assays indicated that miR-137 targets EZH2 and LSD1. These results suggest that miR-137 is a tumor suppressor that is repressed in endometrial cancer because the promoter of its gene becomes hypermethylated.
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Registered trials
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