ArticleCancer management and research2020
LncRNA MIR503HG Inhibits Non-Small Cell Lung Cancer Cell Proliferation by Inducing Cell Cycle Arrest Through the Downregulation of Cyclin D1.
Article in Cancer management and research, 2020. 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, 13 citations in OpenAlex.
- Long non-coding RNA H19X as a regulator of mononuclear cell adhesion to the endothelium in systemic sclerosis.Rheumatology (Oxford, England) · 2024Article
- 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
- LncRNA FAM138B inhibits the progression of non-small cell lung cancer through miR-105-5p.Cell cycle (Georgetown, Tex.) · 2023Article
- Loss of MIR503HG facilitates papillary renal cell carcinoma associated lymphatic metastasis by triggering NOTCH1/VEGFC signaling.International journal of biological sciences · 2023Article
- LncRNAs in non-small cell lung cancer: novel diagnostic and prognostic biomarkers.Frontiers in molecular biosciences · 2023Review
- MIR503HG impeded ovarian cancer progression by interacting with SPI1 and preventing TMEFF1 transcription.Aging · 2022Article
- Four Prognosis-Associated lncRNAs Serve as Biomarkers in Ovarian Cancer.Frontiers in genetics · 2021Article
- LncRNAs in Non-Small-Cell Lung Cancer.Non-coding RNA · 2020Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionLncRNA MIR503HG has been reported to participate in liver cancer and ALK-negative anaplastic large-cell lymphoma, while its role in non-small cell lung cancer (NSCLC) is unknown. We therefore investigated the functions of lncRNA MIR503HG in NSCLC.
methodsMIR503HG expression in paired cancer and non-cancer tissues from NSCLC patients was analyzed by RT-qPCR. The interaction between cyclin D1 and MIR503HG was analyzed by overexpression experiments. Cell cycle analysis was performed by flow cytometry. Cell proliferation was analyzed by CCK-8 assay.
resultsMIR503HG was downregulated in NSCLC and low levels of MIR503HG were associated with poor survival. In contrast, cyclin D1 was upregulated in NSCLC, and cyclin D1 and MIR503HG were inversely correlated. In NSCLC cells, overexpression experiments revealed that MIR503HG functioned as an upstream inhibitor of cyclin D1. MIR503HG overexpression led to G1 cell cycle arrest, while overexpression of cyclin D1 attenuated the effects of MIR503HG overexpression. Similarly, MIR503HG overexpression resulted in reduced cell proliferation rate, while overexpression of cyclin D1 caused the increased cell proliferation rate and attenuated effects of MIR503HG overexpression.
conclusionMIR503HG inhibits NSCLC cell proliferation by inducing cell cycle arrest through the downregulation of cyclin D1.
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