ArticleBMC genomics2015
miR-503 represses human cell proliferation and directly targets the oncogene DDHD2 by non-canonical target pairing.
Article in BMC genomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- The Mechanisms of miRNAs on Target Regulation and their Recent Advances in Atherosclerosis.Current medicinal chemistry · 2024Review
- MicroRNAs as Targets for Cancer Diagnosis: Interests and Limitations.Advanced pharmaceutical bulletin · 2023Review
- Circular RNA circRUNX1 promotes papillary thyroid cancer progression and metastasis by sponging MiR-296-3p and regulating DDHD2 expression.Cell death & disease · 2021Article
- Dysregulation of microRNA Modulatory Network in Abdominal Aortic Aneurysm.Journal of clinical medicine · 2020Article
- Screening of differentially expressed miRNAs in tensile strain‑treated HepG2 cells by miRNA microarray analysis.Molecular medicine reports · 2020Article
- MiR-199a-5p suppresses non-small cell lung cancer via targeting MAP3K11.Journal of Cancer · 2019Article
- Identifying a miRNA signature for predicting the stage of breast cancer.Scientific reports · 2018Article
- microRNA-503 suppresses the migration, proliferation and colony formation of prostate cancer cells by targeting tumor protein D52 like 2.Experimental and therapeutic medicine · 2018Article
- Genome-Wide Maps of m6A circRNAs Identify Widespread and Cell-Type-Specific Methylation Patterns that Are Distinct from mRNAs.Cell reports · 2017Article
- MicroRNA-503 inhibits the proliferation and invasion of breast cancer cells via targeting insulin-like growth factor 1 receptor.Molecular medicine reports · 2017Article
- Multitype Network-Guided Target Controllability in Phenotypically Characterized Osteosarcoma: Role of Tumor Microenvironment.Frontiers in immunology · 2017Article
- An integrative transcriptomics approach identifies miR-503 as a candidate master regulator of the estrogen response in MCF-7 breast cancer cells.RNA (New York, N.Y.) · 2016Article
- Effect of miR-503 Down-Regulation on Growth and Invasion of Esophagus Carcinoma and Related Immune Function.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- MiR-503 inhibited cell proliferation of human breast cancer cells by suppressing CCND1 expression.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- MIR-520f Regulated Itch Expression and Promoted Cell Proliferation in Human Melanoma Cells.Dose-response : a publication of International Hormesis SocietyArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe pathways regulating the transition of mammalian cells from quiescence to proliferation are mediated by multiple miRNAs. Despite significant improvements in our understanding of miRNA targeting, the majority of miRNA regulatory networks are still largely unknown and require experimental validation.
resultsHere we identified miR-503, miR-103, and miR-494 as negative regulators of proliferation in primary human cells. We experimentally determined their genome wide target profiles using RNA-induced silencing complex (RISC) immunoprecipitations and gene expression profiling. Analysis of the genome wide target profiles revealed evidence of extensive regulation of gene expression through non-canonical target pairing by miR-503. We identified the proto-oncogene DDHD2 as a target of miR-503 that requires pairing outside of the canonical 5' seed region of miR-503, representing a novel mode of miRNA-target pairing. Further bioinformatics analysis implicated miR-503 and DDHD2 in breast cancer tumorigenesis.
conclusionsOur results provide an extensive genome wide set of targets for miR-503, miR-103, and miR-494, and suggest that miR-503 may act as a tumor suppressor in breast cancer by its direct non-canonical targeting of DDHD2.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.