ArticleAging2022
MIR503HG impeded ovarian cancer progression by interacting with SPI1 and preventing TMEFF1 transcription.
Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Identification of lncRNAs Deregulated in Epithelial Ovarian Cancer Based on a Gene Expression Profiling Meta-Analysis.International journal of molecular sciences · 2023Pooled it
- LncRNAs in Ovarian Cancer: Emerging Insights and Future Perspectives in Tumor Biology and Clinical Applications.Cancers · 2026Review
- Therapeutic targeting SPI1 in combination with erastin promotes ferroptosis in ccRCC.Communications biology · 2025Article
- TheNon-coding RNA · 2025Article
- Mapping rat lncRNA Bdnf-as.Molecular biology reports · 2025Article
- Article
- Molecular Effects of Glucose onBritish journal of biomedical science · 2025Article
- The oncogenic lncRNA MIR503HG suppresses cellular senescence counteracting supraphysiological androgen treatment in prostate cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- Article
- Potential Clinical Role of LncRNA miR503HG in Multiple Myeloma and its Effect on the Proliferation and Adhesion of Myeloma Cells.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2024Article
- The Role of EMT-Related lncRNAs in Ovarian Cancer.International journal of molecular sciences · 2023Review
- Identification of Chemokine-Related Genes Derived From T and NK Cells in the Tumour Microenvironment of Ovarian Cancer Based on scRNA-Seq.IET systems biologyArticle
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MIR503 host gene (MIR503HG) acts as an important tumor suppressor in many human cancers, but its role and regulatory mechanism in ovarian cancer need to be further studied. In this study, lower expressed MIR503HG was observed in ovarian tumor tissues and cells than in adjacent normal tissues and normal human ovarian epithelial cells. MIR503HG overexpression impaired the proliferative, invasive and EMT properties, and facilitated cell apoptosis in ovarian cancer cells. Nuclear and cytoplasmic separation test suggested that MIR503HG was mainly expressed in the nucleus. RNA immunoprecipitation and RNA pull-down assays confirmed that MIR503HG could bind to transcription factor SPI1 (Spi-1 proto-oncogene), and dual luciferase reporter gene and Chromatin immunoprecipitation assays verified that SPI1 could bind to TMEFF1 (Transmembrane protein with EGF like and two follistatin like domains 1) promoter, suggesting that MIR503HG suppressed TMEFF1 expression by competitively binding SPI1 and blocking transcriptional activation of TMEFF1. Moreover, interference with TMEFF1 reversed the promotion effect of MIR503HG silence on the malignant behaviors of ovarian cancer cells. Moreover, MIR503HG knockdown activated the MAPK and PI3K/AKT pathways by increasing the expression of TMEFF1. In addition, overexpression of MIR503HG
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