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Updated: May 25, 2025

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HDGF Knockout Suppresses Colorectal Cancer Progression and Drug Resistance by Modulating the DNA Damage Response

Riya Su1, Qin Wang1, Qun Hu2

  • 1Department of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China.

Biomolecules
|February 26, 2025
PubMed

Insights

Heparin binding growth factor (HDGF) is overexpressed in colorectal cancer (CRC), promoting tumor growth and drug resistance. Targeting HDGF may offer a novel therapeutic strategy for improving CRC patient outcomes.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Colorectal cancer (CRC) remains a significant health challenge with limited survival improvements despite targeted therapies.
  • Novel therapeutic targets are crucial for enhancing treatment efficacy in CRC patients.

Purpose of the Study:

  • To investigate the role of heparin binding growth factor (HDGF) as a potential therapeutic target in colorectal cancer.
  • To elucidate the molecular mechanisms underlying HDGF's function in CRC progression and drug sensitivity.

Main Methods:

  • Analysis of HDGF expression in CRC tissues and correlation with patient prognosis.
  • Functional studies involving HDGF knockout in CRC cells to assess proliferation, migration, invasion, and apoptosis.
  • Investigation of HDGF's role in DNA damage response, homologous recombination repair, and interaction with CtIP.

Main Results:

  • HDGF is highly expressed in CRC, with overexpression linked to a poorer disease-free interval.
  • HDGF knockout significantly inhibits CRC cell proliferation, migration, and invasion, while promoting apoptosis.
  • HDGF modulates DNA damage response by facilitating homologous recombination repair via CtIP recruitment, impacting CRC drug sensitivity.

Conclusions:

  • HDGF is a validated therapeutic target for colorectal cancer.
  • HDGF's involvement in DNA repair mechanisms, particularly in transcriptionally active genes, highlights its role in maintaining genomic stability in CRC.
  • Targeting HDGF presents a promising strategy for novel CRC therapies.
Keywords:
DNA damage responseH3K36me3HDGFcolorectal cancerhomologous recombination

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