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FAXC interacts with ANXA2 and SRC in mitochondria and promotes tumorigenesis in cholangiocarcinoma

Haruna Fujimori1, Mao Shima-Nakamura1, Shin-Ichiro Kanno2

  • 1Division of Cancer Stem Cell, Miyagi Cancer Center Research Institute, Natori, Japan.

Cancer Science
|March 13, 2024
PubMed

Insights

Researchers identified a novel gene, failed axon connection homolog (FAXC), crucial for cholangiocarcinoma (CCA) tumor growth. Targeting FAXC may offer new therapeutic strategies for this difficult-to-treat cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cholangiocarcinoma (CCA) presents limited therapeutic options due to poorly understood driver genes.
  • Identifying novel targets is critical for advancing CCA treatment strategies.

Purpose of the Study:

  • To identify novel genes involved in CCA tumorigenesis.
  • To elucidate the functional role of failed axon connection homolog (FAXC) in CCA.

Main Methods:

  • Analysis of serially passaged CCA xenograft models.
  • Gene knockdown experiments to assess tumorigenicity.
  • Protein complex analysis (FAXC/ANXA2/c-SRC).
  • Transcriptome analysis of CCA cell lines.

Main Results:

  • FAXC knockdown significantly reduced CCA subcutaneous tumorigenicity in mice.
  • FAXC forms a complex with tumor-promoting genes annexin A2 (ANXA2) and c-SRC in mitochondria.
  • FAXC promotes SRC-dependent ANXA2 phosphorylation at tyrosine-24, requiring specific C-terminal residues.
  • FAXC expression correlates with epithelial-mesenchymal transition, hypoxia, and KRAS signaling pathways in CCA.

Conclusions:

  • FAXC plays a significant role in CCA tumorigenesis.
  • The FAXC/ANXA2/c-SRC complex represents a potential therapeutic target.
  • Understanding FAXC's function provides insights into CCA progression and identifies new avenues for treatment.
Keywords:
ANXA2FAXCSRCcholangiocarcinomatumorigenicity

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