ArticleFrontiers in oncology2021
The LncRNA MIR503HG/miR-224-5p/TUSC3 Signaling Cascade Suppresses Gastric Cancer Development
Article in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- miR-224-5p Suppresses Non-Small Cell Lung Cancer via IL6ST-Mediated Regulation of the JAK2/STAT3 Pathway.Thoracic cancer · 2025Article
- The oncogenic lncRNA MIR503HG suppresses cellular senescence counteracting supraphysiological androgen treatment in prostate cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- Long non-coding RNA-mediated modulation of endoplasmic reticulum stress under pathological conditions.Journal of cellular and molecular medicine · 2024Review
- Shedding light on function of long non-coding RNAs (lncRNAs) in glioblastoma.Non-coding RNA research · 2024Review
- 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
- Stressing the Regulatory Role of Long Non-Coding RNA in the Cellular Stress Response during Cancer Progression and Therapy.Biomedicines · 2022Review
- Inhibition of ITGB1-DT expression delays the growth and migration of stomach adenocarcinoma and improves the prognosis of cancer patients using the bioinformatics and cell model analysis.Journal of gastrointestinal oncology · 2022Article
- NORAD-sponged miR-378c alleviates malignant behaviors of stomach adenocarcinoma via targeting NRP1.Cancer cell international · 2022Article
- Epithelial-mesenchymal transition-related long noncoding RNAs in gastric carcinoma.Frontiers in molecular biosciences · 2022Review
- Neutrophil Extracellular Traps (NETs) Promote Non-Small Cell Lung Cancer Metastasis by Suppressing lncRNA MIR503HG to Activate the NF-κB/NLRP3 Inflammasome Pathway.Frontiers in immunology · 2022Article
- Knockdown ofMolecular medicine reports · 2021Article
- Screening and Comprehensive Analysis of Cancer-Associated tRNA-Derived Fragments.Frontiers in genetics · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundUnfolded protein response (UPR)-mediated tumor-promoting functions have been identified in multiple cancers, and this study focused on investigating the role and molecular mechanisms of UPR in modulating gastric cancer (GC) pathogenesis.
methodsThe bioinformatics analysis was performed to examine the expression status of cancer associated genes in patients with stomach adenocarcinoma (STAD) and predict the targeting sites of miR-224-5p with LncRNA MIR503HG and TUSC3. Genes expressions were quantified by Real-Time qPCR, Western Blot and immunohistochemistry (IHC). Cell proliferation, viability, apoptosis and mobility were evaluated by MTT assay, trypan blue staining assay, flow cytometer and transwell assay, respectively. The binding sites were validated by dual-luciferase reporter gene system assay.
resultsLncRNA MIR503HG and TUSC3 were downregulated, but miR-224-5p was upregulated in GC tissues and cells, in contrast with their normal counterparts. Further gain- and loss-of-function experiments validated that the malignant phenotypes in GC cells, including cell proliferation, invasion, epithelial-mesenchymal transition (EMT) and tumorigenesis, were negatively regulated by LncRNA MIR503HG. Mechanistically, LncRNA MIR503HG upregulated TUSC3 in GC cells through sponging miR-224-5p, resulting in the repression of GC progression. Finally, we validated that knock-down of ATF6, but not other two branches of UPR (PERK1 and IRE1), partially rescued cell proliferation and EMT in the GC cells with LncRNA MIR503HG overexpression.
conclusionsTargeting the LncRNA MIR503HG/miR-224-5p/TUSC3 signaling cascade suppressed ATF6-mediated UPR, resulting in the blockage of GC development.
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