Abstract
Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer that lacks expression of estrogen, progesterone, and HER2 receptors, limiting the effectiveness of targeted therapies and making chemotherapy the primary treatment option. However, resistance to chemotherapy remains a major clinical challenge, often driven by dysregulation of the transforming growth factor-β (TGF-β) signaling pathway. TGF-β plays a dual role in cancer, initially acting as a tumor suppressor but later promoting tumor progression through mechanisms such as epithelial–mesenchymal transition (EMT), immune evasion, and the establishment of cancer stemness. This review aims to explore the role of TGF-β signaling and EMT in mediating drug resistance in TNBC, and to evaluate the potential of β-glucan, a natural immunomodulatory polysaccharide, as a complementary therapeutic agent for this condition. Findings suggest that β-glucan enhances not only antitumor immunity through activation of Dectin-1 and downstream signaling but also suppresses TGF-β-mediated immunosuppressive effects within the tumor microenvironment. These properties position β-glucan as a promising adjuvant candidate for overcoming chemoresistance in triple-negative breast cancer (TNBC). Further experimental and clinical investigations are needed to validate its role in modulating TGF-β signaling and restoring chemosensitivity in tumor cells that are resistant to treatment.
Recommended Citation
Hayati, Hanifa Dinda; Amalia, Riezki; Utama, Gemilang Lara; and Destiani, Dika Pramita
(2025)
"β-Glucan as a Potential Modulator of TGF-β Signaling and EMT-Driven Resistance in Triple-Negative Breast Cancer,"
Pharmacology and Clinical Pharmacy Research: Vol. 10:
Iss.
3, Article 5.
Available at:
https://journal.unpad.ac.id/pcpr/vol10/iss3/5
Included in
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