ArticleJournal of gastrointestinal oncology2022
Circ_0007099 upregulates GNG7 to function as a tumor inhibitor in gastric carcinoma by interacting with miR-425-3p.
Article in Journal of gastrointestinal oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- A prognostic model for gastric cancer based on histamine-associated prognostic genes.Hereditas · 2026Article
- GNG7 as a tumor-suppressor gene in lung adenocarcinoma: implications for prognosis and immune-based therapies.Frontiers in oncology · 2025Article
- Biological disturbance of MiR-425 and its application prospects in cardiovascular diseases.Frontiers in cell and developmental biology · 2025Review
- Circular RNAs-mediated angiogenesis in human cancers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2023Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Circular RNAs (circRNAs) are usually dysregulated in human tumors and affect the malignant progression of tumors. Circ_0007099 is known to be downregulated in gastric carcinoma (GC), and this research was performed to investigate the regulatory function of circ_0007099 in GC progression. Methods: The detection of circ_0007099, miR-425-3p, and G protein γ subunit 7 (GNG7) was performed via reverse transcription-quantitative polymerase chain reaction assay. Cell proliferation was determined by EdU and colony formation assays, and angiogenesis was assessed via a tube formation assay. Glucose metabolism was evaluated with commercial kits, and protein expression was measured by western blot. Dual-luciferase reporter and RNA immunoprecipitation assays were performed to validate the target interaction. An in vivo exploration of circ_0007099 was conducted using a xenograft tumor assay. Results: Circ_0007099 was downregulated in GC patients and cells. Overexpression of circ_0007099 repressed cell proliferation, angiogenesis, and glucose metabolism while enhancing apoptosis in GC cells. Circ_0007099 exhibited a sponge effect on miR-425-3p, and the anti-tumor function of circ_0007099 was achieved by sponging miR-425-3p. Furthermore, miR-425-3p directly targeted GNG7, and miR-425-3p inhibition suppressed malignant progression by reducing GNG7 expression in GC cells. Circ_0007099 sponged miR-425-3p to upregulate the level of GNG7. We also found that Conclusions: This study demonstrated that circ_0007099 inhibits the malignant behavior of GC cells by binding to miR-425-3p, thus regulating the expression of GNG7.
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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.