ArticleBioengineered2022
Downregulation of circular RNA circ-HN1 suppressed the progression of gastric cancer through the miR-485-5p/GSK3A pathway.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Endoplasmic reticulum stress-related genes play a role in the prognosis of lung adenocarcinoma.Discover oncology · 2025Article
- The role of curcumin in modulating circular RNAs and long non-coding RNAs in cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Knocking Down HN1 Blocks Helicobacter pylori-Induced Malignant Phenotypes in Gastric Mucosal Cells and Inhibits Gastric Cancer Cell Proliferation, Cytoskeleton Remodeling, and Migration.Biochemical genetics · 2025Article
- Non-Coding RNA as Biomarkers and Their Role in the Pathogenesis of Gastric Cancer-A Narrative Review.International journal of molecular sciences · 2024Review
- Role of circular RNAs and gut microbiome in gastrointestinal cancers and therapeutic targets.Non-coding RNA research · 2024Review
- Noncoding RNAs and hyperthermic intraperitoneal chemotherapy in advanced gastric cancer.Bioengineered · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gastric cancer (GC) is a malignancy with high incidence and mortality globally. Circular RNAs (circRNAs) are reported to regulate cellular processes in human diseases, including GC. Herein, the functions of circ-HN1 and its molecular mechanisms were investigated. circ-HN1, miR-485-5p, and GSK3A levels in GC were measured using Real time-quantitative polymerase chain reaction (RT-qPCR). Cell proliferation was analyzed using cell counting kit-8 (CCK-8) and colony formation assays. Meanwhile, the migration and invasion abilities were analyzed using the transwell assay. The targeted relationship was confirmed using a luciferase reporter assay and an RNA pull-down assay. In both GC tissues and cells, circ-HN1 expression was upregulated, and its silencing suppressed cellular processes. Moreover, circ-HN1 served as a sponge of miR-485-5p, which was reduced in patients with GC and negatively regulated by circ-HN1 in GC cells. Inhibition of miR-485-4p abolished the biological functions induced by the silencing of circ-HN1. Additionally, miR-485-5p targeted GSK3A in GC, whose expression was elevated in tumor tissues and was negatively correlated with miR-485-5p in tumor cells. GSK3A rescued the inhibition of miR-485-5p in the cellular processes. In conclusion, silencing of the circ-HN1-miR-485-5p-GSK3A regulatory network inhibited GC cell proliferation, migration, and invasion, suggesting that circ-HN1 is a potential target for GC therapy.
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