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Published on: September 30, 2016

MFN2 inhibits colorectal cancer tumorigenesis by regulating glycolysis through TRIM21-mediated PFKP stability

Huiyuan Jiang1, Hongwei Guo1, Yan Wang2

  • 1Department of Colorectal Surgery, Shanxi Province Cancer Hospital, Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences, Cancer Hospital Affiliated to Shanxi Medical University, Taiyuan, Shanxi 030012, China.

Molecular Immunology
|August 1, 2026
PubMed
Abstract

Insights

Mitofusin-2 (MFN2) suppresses colorectal cancer (CRC) growth by reducing glycolysis. Overexpressing MFN2 enhances TRIM21-mediated PFKP degradation, offering a new therapeutic target for CRC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metabolism

Background:

  • Colorectal cancer (CRC) is a leading cause of cancer mortality worldwide.
  • Tumor cell metabolism, particularly glucose metabolism, significantly influences cancer progression.
  • Mitofusin-2 (MFN2) is implicated in cellular glycolysis, suggesting its potential role in CRC.

Purpose of the Study:

  • To investigate the role of Mitofusin-2 (MFN2) in colorectal cancer (CRC) progression.
  • To elucidate the molecular mechanisms by which MFN2 affects CRC cell behavior and tumor growth.
  • To explore the therapeutic potential of targeting MFN2 in CRC.

Main Methods:

  • Analysis of gene expression datasets (GSE143939, GSE81558, GSE184093) and TCGA data for MFN2 expression in CRC.
  • In vitro assays to assess the impact of MFN2 on CRC cell proliferation, apoptosis, and migration.
  • In vivo studies using a xenograft model to evaluate MFN2's effect on tumor growth.
  • Molecular mechanism investigation using co-immunoprecipitation, immunofluorescence, and western blotting.

Main Results:

  • MFN2 was found to be significantly downregulated in CRC tissues and cell lines.
  • MFN2 overexpression reduced glycolysis, inhibited proliferation and migration, and induced apoptosis in CRC cells in vitro.
  • MFN2 overexpression suppressed tumor growth in vivo.
  • MFN2 interacts with PFKP and promotes TRIM21-mediated PFKP degradation, thereby inhibiting CRC progression.

Conclusions:

  • MFN2 overexpression suppresses CRC cell glycolysis and tumor growth.
  • The MFN2/TRIM21/PFKP axis represents a novel mechanism regulating CRC progression.
  • Targeting the MFN2/TRIM21/PFKP pathway could be a promising therapeutic strategy for CRC.
Keywords:
Colorectal cancerGlycolysisMFN2PFKPTRIM21

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