Intercellular interaction dictates cancer cell ferroptosis via NF2-YAP signalling.

ABSTRACT: Ferroptosis, a cell death process driven by cellular metabolism and iron-dependent lipid peroxidation, has been implicated in diseases such as ischaemic organ damage and cancer^1,2. The enzyme glutathione peroxidase 4 (GPX4) is a central regulator of ferroptosis, and protects cells by neutralizing lipid peroxides, which are by-products of cellular metabolism. The direct inhibition of GPX4, or indirect inhibition by depletion of its substrate glutathione or the building blocks of glutathione (such as cysteine), can trigger ferroptosis³. Ferroptosis contributes to the antitumour function of several tumour suppressors such as p53, BAP1 and fumarase^4-7. Counterintuitively, mesenchymal cancer cells-which are prone to metastasis, and often resistant to various tre

SUBMITTER: Wu J 

PROVIDER: S-EPMC6697195 | biostudies-literature | 2019 Aug

REPOSITORIES: biostudies-literature