Related Experiment Video

Updated: Jun 13, 2025

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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
PubMed

Insights

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.
Keywords:
EIF3BKRAS mutationPI3K/AKT signalingTBK1 signalingcolon adenocarcinomacolorectal cancer

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