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Updated: Nov 2, 2025

Cancer-Associated Fibroblasts from Mouse Mammary Tumors as Tools for Molecular and Computational Studies
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PPFIA4 Promotes Colon Cancer Cell Proliferation and Migration by Enhancing Tumor Glycolysis.

Jia Huang1, Meiling Yang2, Zhaoxia Liu1

  • 1Department of Gastroenterology, The Affiliated Nanhua Hospital, Hengyang Medical College, University of South China, Hengyang, China.

Frontiers in Oncology
|June 7, 2021
PubMed
Summary

PPFIA4 is a glycolysis-related oncogene that promotes colon cancer growth and metastasis. Targeting PPFIA4, PFKFB3, and ENO2 may offer new strategies for colon cancer treatment.

Keywords:
PFKFB3/ENO2PPFIA4colon cancerglycolysisinvasion

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Dysregulated glycolysis fuels cancer cell growth and metastasis.
  • The role of PPFIA4 in colon cancer progression requires further elucidation.

Purpose of the Study:

  • To characterize the PPFIA4 gene as a glycolysis-related oncogene in colon cancer.
  • To investigate the mechanism by which PPFIA4 promotes colon cancer cell proliferation and migration.

Main Methods:

  • Bioinformatic analysis using The Cancer Genome Atlas (TCGA) and Gene Expression Profiling Interactive Analysis (GEPIA).
  • In vitro experiments involving PPFIA4 overexpression and knockdown of PFKFB3 and ENO2 in colon cancer cells.

Main Results:

  • PPFIA4 expression and methylation were elevated in colon cancer tissues, correlating with poor patient survival and advanced clinical stages.
  • PPFIA4 overexpression enhanced colon cancer cell viability, migration, invasion, and upregulated epithelial-mesenchymal transition (EMT) markers and glycolysis.
  • PPFIA4 positively correlated with PFKFB3 and ENO2 levels; their knockdown inhibited cancer cell proliferation, migration, invasion, and glycolysis.

Conclusions:

  • PPFIA4 is a potential biomarker for colon cancer, promoting proliferation, migration, invasion, and glycolysis.
  • PPFIA4-mediated upregulation of PFKFB3/ENO2 signaling is a key mechanism driving its oncogenic effects in colon cancer.