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European Journal of Clinical Nutrition, 72 (1), 105

Inhibition of ALG3 induces defects in post-translational N-linked glycosylation modifications and leads to excessive lipid accumulation in cancer cells through sterol regulatory element-binding protein (SREBP1)-dependent lipogenesis, inducing immunogenic ferroptosis in cancer cells and promoting a pro-inflammatory microenvironment, thereby enhancing the antitumor immune response[187]

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