Stark Jillian, Yang Jia-Shu, Hsu Victor W, Henry Whitney S
Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, USA; Koch Institute for Integrative Cancer Research, Cambridge, MA, USA.
Division of Rheumatology, Inflammation and Immunity, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Trends Mol Med. 2026 Feb;32(2):99-100. doi: 10.1016/j.molmed.2025.12.005. Epub 2025 Dec 23.
Palma et al. show that melanoma cells adapt to oxidative stress imposed by the lymphatic niche by shifting their dependency from glutathione peroxidase 4 (GPX4) to ferroptosis suppressor protein 1 (FSP1), to protect from ferroptosis. This highlights the importance of the microenvironment in shaping ferroptosis defenses and supports FSP1 as a targetable vulnerability for lymph node metastases.
帕尔马等人表明，黑色素瘤细胞通过将其对谷胱甘肽过氧化物酶4（GPX4）的依赖性转变为铁死亡抑制蛋白1（FSP1），来适应淋巴微环境施加的氧化应激，从而防止铁死亡。这突出了微环境在塑造铁死亡防御中的重要性，并支持将FSP1作为淋巴结转移的一个可靶向的弱点。
