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Synergistic DBNDD1-GDF15 Signaling Activates the NF-κB Pathway to Promote Colorectal Cancer Progression.

Xiaomin Qi1,2,3, Caijuan Bai2,3, Li Dong2,3

  • 1Laboratory Medicine Center, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China.

Molecular Cancer Research : MCR
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Colorectal cancer (CRC) pathogenesis involves the DBNDD1/GDF15/NF-κB pathway. Targeting DBNDD1 shows promise for new CRC precision medicine treatments and improved patient outcomes.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Colorectal cancer (CRC) is a leading cause of cancer death, with its molecular drivers still under investigation.
  • Understanding gene expression patterns is crucial for identifying mechanisms driving CRC pathogenesis.

Purpose of the Study:

  • To identify differentially expressed genes and molecular patterns linked to colorectal cancer development.
  • To discover novel biomarkers and therapeutic targets for CRC.

Main Methods:

  • Analysis of Gene Expression Omnibus (GEO) data from 585 CRC and 329 normal samples.
  • Construction of a weighted gene co-expression network (WGCNA) and LASSO regression for hub gene identification.
  • In vitro and in vivo experimental validation of key genes and signaling pathways.

Main Results:

  • Five CRC-associated modules were identified, enriched in MAPK signaling and cholesterol metabolism.
  • Thirteen hub genes were selected, with DBNDD1 expression correlating with worse overall survival.
  • DBNDD1 promotes CRC via GDF15 induction, leading to constant NF-κB activation, inhibiting proliferation, migration, invasion, and tumor growth.

Conclusions:

  • The DBNDD1/GDF15/NF-κB signaling pathway is a critical driver of colorectal cancer pathogenesis.
  • DBNDD1 represents a potential therapeutic target for precision medicine in CRC treatment.