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Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells
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Immunofluorescence Imaging of DNA Damage and Repair Foci in Human Colon Cancer Cells

Published on: June 9, 2020

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Atractyloside mimics BORIS knockdown to induce DNA damage in colorectal cancer cells

Mengdie Fang1, Yongfei Song1, Juan Ren1

  • 1Center for Molecular Medicine, Zhejiang Academy of Medical Science Hangzhou, Zhejiang, P. R. China.

International Journal of Clinical and Experimental Pathology
|January 18, 2020
PubMed

Insights

The Brother of Regulator of Imprinted Sites (BORIS) is abnormally expressed in colorectal cancer. Targeting BORIS with atractyloside enhances chemotherapy by inducing DNA damage and amplifying 5-FU effects.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Brother of Regulator of Imprinted Sites (BORIS) is abnormally expressed in colorectal cancer, indicating its potential as a diagnostic and prognostic target.
  • Limited knowledge exists regarding BORIS-related signaling pathways and no drugs currently target BORIS directly.

Purpose of the Study:

  • To identify bioactive drugs that can modulate BORIS-related gene expression in colorectal cancer.
  • To investigate the mechanism by which BORIS affects colorectal cancer cells and its potential synergy with existing therapies.

Main Methods:

  • Microarray assay was used to screen gene regulation panels in BORIS-silenced colorectal cancer cells.
  • Connectivity Map (CMap) database was utilized to identify drugs with similar gene expression profiles to BORIS knockdown.
  • Gene Set Enrichment Analysis (GSEA) and H2A.X immunofluorescence staining were employed to assess apoptosis and DNA damage.

Main Results:

  • Atractyloside treatment was identified as a drug that mimics the gene regulatory effects of BORIS knockdown in colorectal cancer cells.
  • Both atractyloside treatment and BORIS knockdown induced XRCC4 expression, suggesting DNA damage.
  • BORIS knockdown was confirmed to induce DNA damage via H2A.X staining.
  • Atractyloside demonstrated synergistic effects with 5-Fluoruracil (5-FU) in suppressing colorectal cancer cell proliferation.

Conclusions:

  • Atractyloside inhibits BORIS downstream pathways, leading to amplified effects of 5-FU by promoting DNA damage.
  • Targeting BORIS with atractyloside represents a potential strategy to enhance colorectal cancer treatment efficacy.
Keywords:
Fluorouracilatractylosidecolorectal neoplasmsmicroarray analysis

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