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We are analyzing https://www.nature.com/articles/s41467-021-25354-4.

Title:
Dysregulated cholesterol homeostasis results in resistance to ferroptosis increasing tumorigenicity and metastasis in cancer | Nature Communications
Description:
Hypercholesterolemia and dyslipidemia are associated with an increased risk for many cancer types and with poor outcomes in patients with established disease. Whereas the mechanisms by which this occurs are multifactorial we determine that chronic exposure of cells to 27-hydroxycholesterol (27HC), an abundant circulating cholesterol metabolite, selects for cells that exhibit increased cellular uptake and/or lipid biosynthesis. These cells exhibit substantially increased tumorigenic and metastatic capacity. Notably, the metabolic stress imposed upon cells by the accumulated lipids requires sustained expression of GPX4, a negative regulator of ferroptotic cell death. We show that resistance to ferroptosis is a feature of metastatic cells and further demonstrate that GPX4 knockdown attenuates the enhanced tumorigenic and metastatic activity of 27HC resistant cells. These findings highlight the general importance of ferroptosis in tumor growth and metastasis and suggest that dyslipidemia/hypercholesterolemia impacts cancer pathogenesis by selecting for cells that are resistant to ferroptotic cell death. High cholesterol has been associated with increased risk of cancer but the underlying mechanism is not completely understood. Here, the authors show that a cholesterol metabolite induces metabolic reprogramming that generates ferroptosis-resistant cancer cells leading to increased tumour growth and metastasis.
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30 years and 10 months (reg. 1994-08-11).

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🌠 Phenomenal Traffic: 5M - 10M visitors per month

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Keywords {🔍}

cells, cancer, pubmed, article, lipid, gpx, google, scholar, cell, data, cas, fig, cholesterol, hcr, breast, increased, supplementary, activity, expression, central, growth, media, metastatic, resistance, ferroptosis, metastasis, resistant, hcc, shown, uptake, hcs, nature, lipids, mice, results, studies, increase, content, treatment, tumors, models, observed, mdamb, bpd, knockdown, inhibitors, min, stress, tumor, experiments,

Topics {✒️}

nature portfolio privacy policy egfr/akt/srebp-1/ldlr-dependent pathway author information authors research design advertising reporting summary data availability time/dose-response growth curves reprints membrane cholesterol access india srebp-dependent lipid/cholesterol uptake span intron/exon boundaries masked nitrile-oxide electrophiles egfr/kras-dependent tumors stimulating cxcr2-dependent recruitment references vrieling source data file liquid chromatography-mass spectrometry author correspondence original author bio-rad iscript kit numerical source data numerical source data low-density lipoprotein receptor specific selenocysteine-trna required g-protein-coupled receptor nature supplementary information p53r270h/+wapcre mouse model cholesterol/lipid synthesis mediated triple-negative breast cancer ching-yi chang & donald cd36-mediated metabolic rewiring ras-driven cancers rely small slow-growing tumors hrp-conjugated secondary antibodies 27-hydroxycholesterol promotes cell-autonomous tolerate lipid-dependent stress breast cancer development er-positive breast tumors published data indicating er-negative cell lines er-negative breast cancers received considerable attention lipid lc-ms analysis canonical wnt signalling cancer cell-extrinsic manner oxysterol 7alpha-hydroxylase gene

Questions {❓}

Do oxysterols control cholesterol homeostasis?
Metabolism during ECM detachment: achilles heel of cancer cells?

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