All articles tagged with #cancer metabolism
Researchers at the University of Lausanne show that cancer cells' ability to bypass glutamine scarcity relies on biotin-activated pyruvate carboxylase; removing biotin disables this bypass, halting growth, and FBXW7 mutations can intensify this vulnerability, suggesting a multi-pathway therapeutic target and explaining why some glutamine-blocking treatments fail.
Scientists at the University of Lausanne found that some cancers can keep growing with low glutamine by using a biotin-dependent pathway via pyruvate carboxylase. When the FBXW7 gene is mutated, this bypass is diminished, making cells more glutamine-dependent and explaining resistance to anti-glutamine therapies. The work suggests designing treatments that target multiple metabolic pathways at once.
New research from Tokyo University of Science shows polyamines—long linked to anti-aging effects via autophagy and mitochondria—can promote cancer by upregulating the translation factor eIF5A2 and boosting glycolysis, while altering ribosomal protein production. The study found polyamines lift suppression of eIF5A2 by miR-6514-5p, activating a cancer-promoting program distinct from eIF5A1’s aging-related role, suggesting context matters for polyamine supplements and identifying a potential target for cancer therapy.
The study demonstrates that combining a diet free of proline and arginine with the polyamine synthesis inhibitor DFMO significantly suppresses neuroblastoma growth in mouse models by depleting polyamines, inducing tumor differentiation, and disrupting translation at specific codons, offering a promising therapeutic strategy for this childhood cancer.
The study reveals that cancer cells can produce cytosolic acetyl-CoA from β-hydroxybutyrate (β-OHB) via two pathways: the mitochondrial citrate-dependent route involving OXCT1 and a citrate-independent route involving AACS, supporting tumor growth especially under nutrient-limited conditions.
Scientists discovered that glioblastoma brain tumors in mice grow more slowly when deprived of the amino acid serine, revealing a potential metabolic vulnerability that could be targeted for therapy. The tumors typically steal nutrients like serine from their environment to support rapid growth, but a serine-deficient diet slowed tumor progression and extended survival in mice, offering new hope for treatment strategies.
Scientists from Osaka Metropolitan University discovered that a compound in ginger called EMC can inhibit cancer growth by disrupting fatty acid synthesis, revealing a new potential target for cancer therapy and expanding understanding of cancer metabolism beyond the traditional Warburg effect.