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Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
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EIF3B Promotes KRAS Gene Mutation-Driven Colon Adenocarcinoma Progression Through the TBK1 and PI3K/AKT Signaling
Chongren Ren1, Yaxin Qin1, Dujuan Cao2
1Department of General Surgery, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, China.
Journal of Biochemical and Molecular Toxicology
|June 12, 2025
Summary
Targeting EIF3B shows promise for colorectal cancer (CRC) with KRAS mutations. Inhibiting EIF3B reduces tumor growth and disrupts key signaling pathways in KRAS-mutant colorectal adenocarcinoma.
Area of Science:
- Oncology
- Molecular Biology
- Bioinformatics
Background:
- KRAS mutations drive cancer, necessitating targeted therapies.
- EIF3B is a potential therapeutic target in colorectal cancer (CRC).
Purpose of the Study:
- To investigate the role of EIF3B in KRAS-mutant colorectal adenocarcinoma (COAD).
- To explore EIF3B's interactions and its impact on signaling pathways in KRASmut COAD.
Main Methods:
- Bioinformatics analysis of TCGA data.
- RNA sequencing, RT-qPCR, and Western blot for gene expression.
- RNA immunoprecipitation (RIP) for interaction confirmation.
Main Results:
- Elevated EIF3B and TBK1 mRNA/protein in KRASmut COAD.
- EIF3B silencing inhibited proliferation and disrupted TBK1, PI3K/AKT, and JAK2/STAT3 pathways.
- EIF3B regulated TBK1 and PIK3CA translation.
Conclusions:
- EIF3B is a key regulator in KRASmut COAD progression.
- Targeting EIF3B offers a novel therapeutic strategy for KRASmut COAD.
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