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Fig. 6 | Cancer & Metabolism

Fig. 6

From: Therapy-induced lipid uptake and remodeling underpin ferroptosis hypersensitivity in prostate cancer

Fig. 6

Graphic representation of changes to lipid supply and lipid remodeling that underpin therapy-induced multidrug tolerance and ferroptosis hypersensitivity in PCa cells. In the androgen-stimulated, proliferative state (left), the cellular lipid pool is fueled by both de novo lipogenesis (DNL) of cholesterol (green) and FAs (orange) and lipid uptake. Mitochondrial FA oxidation and TCA cycle activity provide energy and precursor for biomass synthesis. In the therapy-induced quiescent state, DNL is reduced, whereas lipid uptake through cargo-selective (lipid transporters) and non-selective transport mechanisms (tunneling nanotubes and macropinocytosis, MPC) is enhanced. Therapy-induced lipid remodeling includes mobilization of storage lipids (CEs and TAGs) through lipases, increased levels of all major phospholipid species and their enrichment with PUFAs (purple), leading to increased membrane fluidity, lipid peroxidation (LPOx), and GPX4 dependence. Increased and decreased activities are highlighted in red and gray, respectively. Cer, ceramides

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