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Updated: Aug 6, 2026
06:21
Multi-Gene Single Nucleotide Polymorphism Detection in Gastric Cancer Based on Ion Semiconductor Sequencing Platform
Published on: May 10, 2024
m6A-methylated circFANCB Promotes Gastric Cancer Progression by Regulating Cellular Ferroptosis Through
Haifeng Wang1, Yan Li2, Tiantian Sun1
1Department of Oncology, The People's Hospital of Beilun District; Beilun Branch of the First Affiliated Hospital of Medical College of Zhejiang University, Ningbo, China.
Journal of Biochemical and Molecular Toxicology
|July 25, 2026
Summary
Circular FANCB (circFANCB) promotes gastric cancer (GC) progression by inhibiting ferroptosis via the miR-454-3p/CEACAM5 pathway. METTL3 enhances circFANCB, suggesting therapeutic targets for GC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Gastric cancer (GC) is a leading cause of cancer-related mortality globally.
- Circular FANCB (circFANCB) is implicated in various cancers, but its role in GC remains unelucidated.
- Understanding novel molecular mechanisms is crucial for developing effective GC therapies.
Purpose of the Study:
- To investigate the role and mechanism of circFANCB in gastric cancer progression.
- To explore the regulatory pathway involving circFANCB, miR-454-3p, and CEACAM5 in GC.
- To determine the influence of METTL3 on circFANCB expression and its impact on GC.
Main Methods:
- circRNA sequencing, qRT-PCR, and functional assays (proliferation, migration, invasion, angiogenesis, ferroptosis).
- In vivo xenograft mouse models and immunohistochemistry.
- MeRIP, RIP assays, and dual-luciferase reporter assays to investigate m6A modification and interactions.
Main Results:
- circFANCB expression was significantly upregulated in GC tissues and cell lines.
- circFANCB knockdown suppressed GC cell proliferation, migration, invasion, angiogenesis, and promoted cell death.
- circFANCB promotes GC progression by upregulating CEACAM5 via sponging miR-454-3p, thereby inhibiting ferroptosis. METTL3 enhances circFANCB expression via m6A modification.
Conclusions:
- circFANCB acts as an oncogenic circRNA in GC by promoting proliferation and inhibiting ferroptosis through the miR-454-3p/CEACAM5 axis.
- METTL3-mediated m6A modification of circFANCB contributes to GC malignancy.
- circFANCB represents a potential therapeutic target for gastric cancer treatment.
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