ArticleCell cycle (Georgetown, Tex.)
METTL3-mediated circ_0003998 serves as oncogene in non-small cell lung cancer through regulating miR-330-5p/CXCL3 axis.
Article in Cell cycle (Georgetown, Tex.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
2 citing papers in PubMed.
- Research progress of MicroRNA in lung cancer.Discover oncology · 2026Review
- Emerging functions of m6A-modified circRNAs and their targeting strategies in lung cancer.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Circular RNA (circRNA) is involved in the occurrence of many cancers. Nonetheless, the mechanism of circ_0003998 in non-small cell lung cancer (NSCLC) needs to be studied in depth. Real-time quantitative PCR (RT-qPCR) was carried out to check the expression of circ_0003998, microRNA-330-5p (miR-330-5p), chemokine (C-X-C motif) ligand 3 (CXCL3) and methyltransferase-3 (METTL3) in NSCLC tissues and cells. CXCL3, Vimentin and E-cadherin protein levels were measured by western blot. The functions of circ_0003998 in NSCLC cell proliferation, apoptosis, angiogenesis, migration and invasion were tested by clone formation assay, flow cytometry, tube formation assay, wound healing assay, and transwell assay in vitro. The dual-luciferase reporter assay was made to verify the relationship between miR-330-5p and circ_0003998 or CXCL3. Finally, animal experiment was made to further research the function of circ_0003998 on tumor formation in vivo. The interaction between circ_0003998 and METTL3 was analyzed by RNA Immunoprecipitation (RIP) assay, methylated RNA Immunoprecipitation (MeRIP) assay and dual-luciferase reporter assay. In NSCLC tissue and cells, circ_0003998 was markedly overexpressed. Circ_0003998 suppression inhibited NSCLC cell growth, angiogenesis, migration and invasion. Circ_0003998 sponged miR-330-5p, and miR-330-5p inhibitor could reverse the suppression effect of circ_0003998 knockdown on NSCLC cell behaviors. CXCL3 was a downstream target gene of miR-330-5p, and CXCL3 overexpression also reversed the suppressive effect of miR-330-5p on NSCLC cell behaviors. Interference of circ_0003998 reduced NSCLC tumorigenesis by regulating miR-330-5p/CXCL3 axis. Also, METTL3 promoted the expression of circ_0003998 by m6A modification. METTL3-modified circ_0003998 promoted NSCLC cell malignancy through miR-330-5p/CXCL3 axis, suggesting that circ_0003998 might be a new treatment strategy for NSCLC.
Indexed as
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.