Exploring SGLT2 Inhibitors' Activity in Breast Cancer: An Overview
Sodium‒glucose cotransporter 2 (SGLT2) inhibitors have become viable therapeutic options for treating breast cancer. Diabetes is the primary source of these medications. This research examines how SGLT2 blockers can induce apoptosis, decrease the amount of glucose taken up by cancer cells, and modify key signaling pathways, such as the PI3K/AKT/mTOR and MAPK pathways. The effects of four different SGLT2 inhibitors on breast cancer cells were investigated in this study via both in vitro and in vivo testing: dapagliflozin, ipragliflozin, canagliflozin, and empagliflozin. The potential synergistic effects of these inhibitors with conventional chemotherapy medications were also examined. This review explores the complex relationship between SGLT2 inhibitors and breast cancer, examining how drugs interact with this disease at various stages of its development. Additionally, this study highlights how SGLT2 inhibitors may be used in conjunction with precision medicine techniques to treat breast cancer. Although encouraging outcomes have been noted, this review highlights the necessity of additional clinical studies to evaluate the safety and effectiveness of SGLT2 blockers in patients with breast cancer, in addition to ongoing research into the molecular mechanisms underlying the anticancer effects of these drugs.
Authors
- Ritesh Bhole (ORCID: https://orcid.org/0000-0003-4088-7470)
- Harshad S. Kapare (ORCID: https://orcid.org/0000-0003-2991-7413)
- Shailendra Shivaji Gurav (ORCID: https://orcid.org/0000-0001-5564-2121)
- Sonali D. Labhade
- Gayatri S. Maldhure
Institutions
- Goa University (IN)
- Goa Medical College (IN)
- Dr. D. Y. Patil Medical College, Hospital and Research Centre (IN)
- Dr. D.Y. Patil Vidyapeeth, Pune (IN)
Publication Details
- Journal
- Current Topics in Medicinal Chemistry
- Published
- 2025-04-15
- DOI
- https://doi.org/10.2174/0115680266371287250402051235
- Primary Topic
- Diabetes Treatment and Management
- Type
- article
- Field-Weighted Citation Impact
- 0.00