ArticleOncoTargets and therapy2018
The miR-503 cluster is coordinately under-expressed in endometrial endometrioid adenocarcinoma and targets many oncogenes, cell cycle genes, DNA repair genes and chemotherapy response genes.
Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Endometrial cancer progression driven by PTEN-deficiency requires miR-424(322)Cell death & disease · 2025Article
- Application of Cord Blood-Derived Exosomes in Tumor Prevention and Treatment.Clinical Medicine Insights. Oncology · 2025Review
- Particles and Prejudice: Nanomedicine Approaches to Reducing Health Disparities in Endometrial Cancer.Small (Weinheim an der Bergstrasse, Germany) · 2024Review
- The interplay of sex steroid hormones and microRNAs in endometrial cancer: current understanding and future directions.Frontiers in endocrinology · 2023Review
- Review
- Construction of miRNA-mRNA Regulatory Network and Prognostic Signature in Endometrial Cancer.OncoTargets and therapy · 2021Article
- miR-148-3p Inhibits Growth of Glioblastoma Targeting DNA Methyltransferase-1 (DNMT1).Oncology research · 2019Article
- MicroRNAs in porcine uterus and serum are affected by zearalenone and represent a new target for mycotoxin biomarker discovery.Scientific reports · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe miR-503 miRNA cluster, located at Xq23.1, is composed of six miRNAs; miR-424, miR-503, miR-542, miR-450a-1, miR-450a-2 and miR-450b. Numerous studies have focused on the relationship of one or two members of the cluster and various human cancers. Here, we suggest that the entire cluster as a single coordinately expressed polycistron transcribed from a single promoter in endometrial endometrioid adenocarcinoma (EEA). SUBJECTS AND
methodsA tissue panel composed of twenty histologically confirmed endometrial endometrioid adenocarcinomas (EEA) and four benign endometrium was assembled under informed consent. Expression of each member of the miR-503 cluster was determined by quantitative PCR and differences in expression between EEA and benign tissues were assessed via the standard ΔΔCt method. In addition, the role of promoter methylation status in miRNA expression was examined in Ishikawa H cells following exposure to the cytidine analog Decitabine.
resultsExpression of each member of the miR-503 cluster is significantly downregulated in EEA in our tumor sample. Both in our tumor sample and in The Cancer Genome Atlas (TCGA) there is evidence of highly correlated expression further supporting the idea that the miR-503 cluster is a polycistron. Looking at each member of the miR-503 cluster we were able to identify 55 unique experimentally validated target genes which include a substantial number of genes involved in carcinogenesis, DNA damage response, cell cycle regulation and chemotherapeutic response. We also found preliminary evidence that regulation of the miR-503 cluster is governed by methylation of the promoter in EEA.
conclusionThe totality of the data presented here strongly suggest that the miR-503 cluster as a whole merits further investigation as an important potential therapeutic target in EEA.
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