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REVIEW

Targeting Sphingolipids in Breast Cancer: From Tumor Biology to Therapeutic Strategies

Min Hee Kim1, Boyoon Huh1, Joo-Won Park1,*, Woo-Jae Park2,*
1 Department of Biochemistry, College of Medicine, Ewha Womans University, Seoul, 07804, Republic of Korea
2 Department of Biochemistry, Chung-Ang University College of Medicine, Seoul, 06974, Republic of Korea
* Corresponding Author: Joo-Won Park. Email: email; Woo-Jae Park. Email: email
(This article belongs to the Special Issue: Advances in Pathology, Early Diagnosis and Therapeutic Strategies for Breast Cancer)

Oncology Research https://doi.org/10.32604/or.2025.071523

Received 06 August 2025; Accepted 26 November 2025; Published online 24 December 2025

Abstract

Breast cancer is one of the most prevalent malignancies among women and comprises a heterogeneous spectrum of molecular subtypes with distinct biological behaviors. Among various regulatory molecules, sphingolipids play pivotal roles in dynamically modulating fundamental cellular processes such as proliferation, apoptosis, and metastasis through metabolic interconversions, including phosphorylation, glycosylation, and the generation of sphingosine-1-phosphate. This review aims to elucidate the mechanisms through which sphingolipid metabolism orchestrates cancer cell fate and drives breast cancer progression. Particular emphasis is placed on the balance between proapoptotic ceramides and pro-survival metabolites, such as sphingosine-1-phosphate, which collectively influence tumor growth and the therapeutic response. Additional sphingolipid species, including glucosylceramide and gangliosides (GD2, GD3, GM1, and GM3), have also been implicated in promoting breast cancer development. Furthermore, sphingolipid-based therapeutic strategies, including immunotherapy and antibody therapy, are discussed. By providing a comprehensive overview of sphingolipid metabolism, this review aims to identify novel therapeutic targets that may help overcome treatment resistance and improve clinical outcomes in breast cancer.

Keywords

breast cancer; sphingolipid; drug resistance; metastasis; metabolism

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