Alteration of DNA methyltransferases by eribulin elicits broad DNA methylation changes with potential therapeutic implications for triple-negative breast cancer

Epigenomics. 2024 Mar;16(5):293-308. doi: 10.2217/epi-2023-0339. Epub 2024 Feb 15.

Abstract

Background: Triple-negative breast cancer (TNBC) is an aggressive disease with limited treatment options. Eribulin, a chemotherapeutic drug, induces epigenetic changes in cancer cells, suggesting a unique mechanism of action. Materials & methods: MDA-MB 231 cells were treated with eribulin and paclitaxel, and the samples from 53 patients treated with neoadjuvant eribulin were compared with those from 14 patients who received the standard-of-care treatment using immunohistochemistry. Results: Eribulin treatment caused significant DNA methylation changes in drug-tolerant persister TNBC cells, and it also elicited changes in the expression levels of epigenetic modifiers (DNMT1, TET1, DNMT3A/B) in vitro and in primary TNBC tumors. Conclusion: These findings provide new insights into eribulin's mechanism of action and potential biomarkers for predicting TNBC treatment response.

Keywords: DNA methylation; breast cancer; chemotherapy; epigenetic; epithelial-to-mesenchymal transition.

MeSH terms

  • Cell Line, Tumor
  • DNA / metabolism
  • DNA Methylation*
  • Furans*
  • Humans
  • Ketones / pharmacology
  • Ketones / therapeutic use
  • Mixed Function Oxygenases / genetics
  • Polyether Polyketides*
  • Proto-Oncogene Proteins / genetics
  • Triple Negative Breast Neoplasms* / drug therapy
  • Triple Negative Breast Neoplasms* / genetics
  • Triple Negative Breast Neoplasms* / pathology

Substances

  • eribulin
  • Ketones
  • DNA
  • TET1 protein, human
  • Mixed Function Oxygenases
  • Proto-Oncogene Proteins
  • Polyether Polyketides
  • Furans