Boutaina Daher

TL;DR: In vitro pharmacological inhibition of xCT by low concentrations of erastin phenocopied xCT-KO and potentiated the cytotoxic effects of both gemcitabine and cisplatin in PDAC cell lines strongly support that inhibition ofxCT, by its dual induction of nutritional and oxidative cellular stresses, has great potential as an anticancer strategy.

TL;DR: This review reports and discusses the potential therapeutic benefit of disrupting the major Myc/Hypoxia-induced metabolic pathway, also known as fermentative glycolysis or "Warburg effect", in aggressive cancer cell lines and shows how cancer cells exploit metabolic plasticity to survive the metabolic and energetic blockade or arrest their growth.

TL;DR: The present review summarized the metabolic networks involving the amino acid cysteine in cancer and ferroptosis and focused on describing the recently discovered glutathione-independent pathway, a potential player in cancer ferroPTosis resistance.

TL;DR: This is the first comprehensive review focusing on the effects of the cell-to-cell contact/interplay in the development of resistance to ferroptosis, while the contribution of cell-born factors has been summarized previously so here the authors just listed them.

TL;DR: Investigating potential resistance mechanisms that cancer cells with genetically disrupted xCT (xCTKO) may exploit in order to develop resistance to ferroptosis unequivocally showed that the presence of a cysteine/cystine shuttle between neighboring cells is the mechanism that provides redox and nutrient balance, and thus ferroPTotic resistance in xCTKO cells.