ArticleJournal of oncology2021
MicroRNA-552 Accelerates the Progression of Gastric Cancer by Targeting FOXO1 and Regulating PI3K/AKT Pathway.
Article in Journal of oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Overexpression of FOXO1 may suppress proliferation and migration and correlate with tumor immune cells in nasopharyngeal carcinoma.Translational cancer research · 2026Article
- FOXO1 in cancer: context-dependent roles, microRNA regulation, and therapeutic opportunities.Discover oncology · 2026Review
- FOXO1 phosphorylation as a context-dependent molecular switch in cancer: from mechanisms to precision therapy.World journal of surgical oncology · 2025Review
- Identification and potential mechanism of a novel gastric cancer suppressor tRF-24-6VR8K09LE9.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Integration of TE Induces Cancer Specific Alternative Splicing Events.International journal of molecular sciences · 2022Review
- The FOXO family of transcription factors: key molecular players in gastric cancer.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Extracellular Matrix-Associated Pathways Promote the Progression of Gastric Cancer by Impacting the Dendritic Cell Axis.International journal of general medicine · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The specific function of microRNA-552 (miR-552) has been investigated in several malignancies, except gastric cancer (GC). Therefore, this study was performed to determine the role of miR-552 in GC.GC tissues and adjacent non-tumor tissues were collected to determine the expressions of miR-552. Quantitative real-time polymerase chain reaction assays (RT-qPCR) and Western blot analysis were carried out to measure expression levels. The regulatory mechanism of miR-552 was explored by (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) MTT Assay, and Transwell assays. The binding site between miR-552 and FOXO1 was verified by dual-luciferase reporter assays. Upregulation of miR-552 expression was detected and associated with worse clinical outcomes in GC. Furthermore, high miR-552 expression predicted poor prognosis in GC patients. Functionally, upregulation of miR-552 promoted cell viability, metastasis, epithelial-mesenchymal transition (EMT), and phosphatidylinositol 3-kinase and protein kinase B (PI3K/AKT) pathway in GC. In addition, miR-552 was confirmed to target forkhead box O1 (FOXO1) directly and inversely regulate its expression in GC. Upregulation of FOXO1 reversed the carcinogenesis of miR-552 in GC. In conclusion, miR-552 serves as a tumor promoter in GC through targeting FOXO1 and regulating EMT and PI3K/AKT pathway.
Identifiers
What OpenQuestion holds
Registered trials
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.