Functional exploration of copy number alterations in a Drosophila model of triple-negative breast cancer

Dis Model Mech. 2024 Jul 1;17(7):dmm050191. doi: 10.1242/dmm.050191. Epub 2024 Jul 3.

Abstract

Accounting for 10-20% of breast cancer cases, triple-negative breast cancer (TNBC) is associated with a disproportionate number of breast cancer deaths. One challenge in studying TNBC is its genomic profile: with the exception of TP53 loss, most breast cancer tumors are characterized by a high number of copy number alterations (CNAs), making modeling the disease in whole animals challenging. We computationally analyzed 186 CNA regions previously identified in breast cancer tumors to rank genes within each region by likelihood of acting as a tumor driver. We then used a Drosophila p53-Myc TNBC model to identify 48 genes as functional drivers. To demonstrate the utility of this functional database, we established six 3-hit models; altering candidate genes led to increased aspects of transformation as well as resistance to the chemotherapeutic drug fluorouracil. Our work provides a functional database of CNA-associated TNBC drivers, and a template for an integrated computational/whole-animal approach to identify functional drivers of transformation and drug resistance within CNAs in other tumor types.

Keywords: Drosophila; Genomics; Triple-negative breast cancer.

MeSH terms

  • Animals
  • Cell Transformation, Neoplastic / genetics
  • DNA Copy Number Variations* / genetics
  • Disease Models, Animal*
  • Drosophila melanogaster / genetics
  • Drug Resistance, Neoplasm / genetics
  • Female
  • Fluorouracil / pharmacology
  • Fluorouracil / therapeutic use
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Triple Negative Breast Neoplasms* / genetics
  • Triple Negative Breast Neoplasms* / pathology
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Tumor Suppressor Protein p53
  • Fluorouracil