Previous studies have reported that hypoxia-inducible factor (HIF)-1α confers endocrine resistance and that zoledronic acid (ZOL) decreases HIF‑1α expression in estrogen receptor‑positive breast cancer.
Activation of hypoxia-inducible factor-1α by prolonged in vivo hyperinsulinemia treatment potentiates cancerous progression in estrogen receptor-positive breast cancer cells.
HIF-1α is a determinant of resistance to endocrine therapy and should be considered as a potential therapeutic target for overcoming endocrine resistance in estrogen receptor (ER)-positive breast cancer.
Since both HIF-1alpha and ER are highly active in the ER-positive breast cancer, C Delta553 has the potential to be developed as a protein drug to treat breast cancer by blocking these two signaling pathways.