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FAXC depletion contributes to tumor progression via the c-MET pathway in renal cell carcinoma

Masato Konno1, Haruna Fujimori2, Shin-Ichiro Kanno3

  • 1Division of Cancer Stem Cell, Miyagi Cancer Center Research Institute, 47-1 Nodayama, Medeshima-Shiote, Natori, Miyagi, 981-1293, Japan; Division of Urology, Miyagi Cancer Center, 47-1 Nodayama, Medeshima-Shiote, Natori, Miyagi, 981-1293, Japan; Department of Urology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, Miyagi, 980-8574, Japan.

Biochemical and Biophysical Research Communications
|July 24, 2025
PubMed

Insights

Failed Axon Connections Homolog (FAXC) gene depletion accelerates renal cell carcinoma (RCC) proliferation by activating c-MET signaling. FAXC downregulation in tumors suggests a tumor-suppressive role for FAXC in kidney cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Renal cell carcinoma (RCC) is the most common kidney cancer.
  • Novel therapeutic targets are needed to improve RCC patient outcomes.
  • The Failed Axon Connections Homolog (FAXC) gene is a potential cancer target.

Purpose of the Study:

  • Investigate the role of the FAXC gene in RCC.
  • Determine the relationship between FAXC and c-MET signaling in RCC.
  • Evaluate FAXC expression in RCC patient specimens.

Main Methods:

  • FAXC knockdown and overexpression in RCC cell lines.
  • Assessment of cell proliferation rates.
  • Analysis of c-MET expression and phosphorylation.
  • Mitochondrial localization studies of FAXC.
  • Correlation analysis in RCC patient tumor and adjacent normal tissues.

Main Results:

  • FAXC knockdown increased RCC cell proliferation and c-MET activation.
  • FAXC overexpression reduced RCC cell proliferation and c-MET expression.
  • FAXC is localized to mitochondria in RCC cells.
  • FAXC expression was downregulated in RCC tumors and negatively correlated with c-MET phosphorylation.

Conclusions:

  • FAXC acts as a tumor suppressor in RCC.
  • FAXC depletion promotes RCC cell proliferation via c-MET pathway activation.
  • FAXC may represent a novel therapeutic target for kidney cancer.
Keywords:
FAXCRenal cell carcinomac-MET

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