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CD44 and SLC1A2 are commonly regulated but do not form a fusion transcript in ER+ breast cancer

Francesca Bonechi1, Marina Bacci2, Nicla Lorito1

  • 1Department of Experimental and Clinical Biomedical Sciences, University of Florence, Viale Morgagni 50, 50134, Florence, Italy.

Molecular and Cellular Biochemistry
|May 23, 2025
PubMed

Insights

This study found no CD44-SLC1A2 gene fusions in endocrine therapy-resistant breast cancer. However, high CD44/SLC1A2 expression and altered amino acid metabolism were linked to poor outcomes, suggesting new therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Metabolic Research

Background:

  • Endocrine therapy (ET) is a cornerstone for ER+ HER2- breast cancer.
  • Therapeutic resistance to ET poses a significant clinical challenge in breast cancer management.
  • CD44-SLC1A2 gene fusions are implicated in gastrointestinal malignancies.

Purpose of the Study:

  • To investigate the potential role of CD44-SLC1A2 gene fusions in endocrine therapy resistance in breast cancer.
  • To explore the association between CD44 and SLC1A2 expression and patient survival.
  • To identify metabolic vulnerabilities in therapy-resistant breast cancer subpopulations.

Main Methods:

  • Analysis of CD44-SLC1A2 gene fusions in breast cancer samples.
  • Correlation of CD44 and SLC1A2 gene expression with survival data.
  • Metabolic profiling of therapy-resistant breast cancer subpopulations.

Main Results:

  • No CD44-SLC1A2 gene fusions were detected in the studied breast cancer cohort.
  • High expression levels of CD44 and SLC1A2 were significantly associated with poorer patient survival outcomes.
  • A therapy-resistant subpopulation was identified, relying on aspartate and glutamate metabolism.

Conclusions:

  • CD44-SLC1A2 gene fusions do not appear to be a mechanism of ET resistance in this breast cancer cohort.
  • Elevated CD44 and SLC1A2 expression may serve as biomarkers for poor prognosis in ER+ HER2- breast cancer.
  • Targeting aspartate and glutamate metabolism presents a potential therapeutic strategy for overcoming ET resistance.
Keywords:
Breast cancerEndocrine therapyMetabolic reprogramming

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