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Updated: Dec 25, 2025

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Integrative analysis of genomic amplification-dependent expression and loss-of-function screen identifies ASAP1 as a

Jichao He1, Ronan P McLaughlin1, Lambert van der Beek1

  • 1Division of Drug Discovery and Safety, Leiden Academic Centre for Drug Research, Leiden University, 2300 RA, Leiden, The Netherlands.

Oncogene
|April 3, 2020
PubMed

Insights

Triple-negative breast cancer (TNBC) lacks targeted therapies. This study identifies ASAP1 as an amplification-driven gene promoting TNBC proliferation and metastasis, suggesting it as a potential therapeutic target for this intractable disease.

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Triple-negative breast cancer (TNBC) is a heterogeneous and aggressive cancer subtype with limited targeted treatment options.
  • Gene amplification, leading to increased gene expression, is a significant driver in tumorigenesis and a potential therapeutic vulnerability.

Purpose of the Study:

  • To identify and validate novel therapeutic targets for TNBC by analyzing amplification-dependent gene expression.
  • To investigate the role of identified candidate genes in TNBC proliferation, survival, and clinical outcomes.

Main Methods:

  • Applied Analytical Multi-scale Identification of Recurring Events (AMIIRE) and transcript quantification to 222 TNBC tumors.
  • Conducted siRNA-based loss-of-function screens to validate candidate driver genes.
  • Analyzed gene copy number gain (CNG) and expression data across large breast cancer datasets (cBioPortal, bc-GenExMiner).

Main Results:

  • Identified 138 candidate genes with copy number gain and correlated gene expression in TNBC.
  • Validated EGFR, MYC, ASAP1, IRF2BP2, and CCT5 as proliferation drivers in TNBC cells.
  • ASAP1 amplification and high expression strongly correlate with poor metastatic relapse-free survival in TNBC patients and modulate key survival signaling pathways.

Conclusions:

  • ASAP1 is an amplification-dependent driver gene in TNBC, promoting proliferation and influencing patient survival.
  • ASAP1's role in modulating cytokine and apoptosis signaling pathways makes it a promising actionable therapeutic target for TNBC treatment.

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