Suppression of Breast Cancer Progression by FBXL16 via Oxygen-Independent Regulation of HIF1α Stability

Researchers found that F-box and leucine-rich repeat protein 16 (FBXL16) acted as a tumor suppressor in TNBCs. FBXL16 directly bound to HIF1α and induced its ubiquitination and degradation, regardless of the tumor microenvironment, resulting in angiogenesis features of breast cancer.