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cells, gpx, tcf, fig, cancer, ferroptosis, pubmed, cell, article, google, scholar, expression, cas, supplementary, signaling, death, gastric, resistance, lipid, cisplatin, wntbetacatenin, data, pylori, central, tumor, mda, tissues, nature, promotes, ags, mice, china, wang, chemotherapy, transcription, pvalues, calculated, shandong, analysis, production, patients, showed, assay, pathway, peroxidation, inhibition, treated, treatment, erastin, hne,

Topics {✒️}

supplementary table s1 supplementary table s2 figure legend nature portfolio supplementary file β-catenin/tcf7l2-dependent transcriptional regulation privacy policy wnt/β-catenin signaling pathway wnt/beta-catenin signaling pathway akt-yb1-mdr1 signaling pathway original author beta-catenin/tcf4 transcription complex targeting wnt/beta-catenin signaling oncogenic-ras-harboring cancer cells advertising wnt/β-catenin signaling β-catenin/tcf4 interaction blocks wnt/β-catenin target genes s5 inhibits wnt/beta-catenin signals wnt/beta-catenin signaling wnt/beta-catenin pathway [14 clinical research center cck-8 solutions nature iron-dependent form regulating β-catenin desumoylation wnt/beta-catenin signals medical research reprints cancer research apoptosis inhibitor z-vad-fmk overcoming hypoxia-induced resistance open-label wnt/β-catenin beta-catenin-coding plasmid beta-catenin intracellular accumulation inverted phase-contrast microscope beta-catenin transient silencing promotes acquired chemo-resistance cisplatin-based chemotherapies remain tcf4-mediated biological functions microbiology/key laboratory limits cystine/gsh import thermo fisher scientific penter-beta-catenin wnt pathway activation social media european economic area iron-dependent accumulation

Questions {❓}

• Can we safely target the WNT pathway?

Schema {🗺️}

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         description:The development of chemotherapy resistance is the most vital obstacle to clinical efficacy in gastric cancer (GC). The dysregulation of the Wnt/beta-catenin signaling pathway is critically associated with GC development and chemotherapy resistance. Ferroptosis is a form of regulated cell death, induced by an iron-dependent accumulation of lipid peroxides during chemotherapy. However, whether the Wnt/beta-catenin signaling directly controls resistance to cell death, remains unclear. Here, we show that the activation of the Wnt/beta-catenin signaling attenuates cellular lipid ROS production and subsequently inhibits ferroptosis in GC cells. The beta-catenin/TCF4 transcription complex directly binds to the promoter region of GPX4 and induces its expression, resulting in the suppression of ferroptotic cell death. Concordantly, TCF4 deficiency promotes cisplatin-induced ferroptosis in vitro and in vivo. Thus, we demonstrate that the aberrant activation of the Wnt/beta-catenin signaling confers ferroptosis resistance and suggests a potential therapeutic strategy to enhance chemo-sensitivity for advanced GC patients.
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      headline:Wnt/beta-catenin signaling confers ferroptosis resistance by targeting GPX4 in gastric cancer
      description:The development of chemotherapy resistance is the most vital obstacle to clinical efficacy in gastric cancer (GC). The dysregulation of the Wnt/beta-catenin signaling pathway is critically associated with GC development and chemotherapy resistance. Ferroptosis is a form of regulated cell death, induced by an iron-dependent accumulation of lipid peroxides during chemotherapy. However, whether the Wnt/beta-catenin signaling directly controls resistance to cell death, remains unclear. Here, we show that the activation of the Wnt/beta-catenin signaling attenuates cellular lipid ROS production and subsequently inhibits ferroptosis in GC cells. The beta-catenin/TCF4 transcription complex directly binds to the promoter region of GPX4 and induces its expression, resulting in the suppression of ferroptotic cell death. Concordantly, TCF4 deficiency promotes cisplatin-induced ferroptosis in vitro and in vivo. Thus, we demonstrate that the aberrant activation of the Wnt/beta-catenin signaling confers ferroptosis resistance and suggests a potential therapeutic strategy to enhance chemo-sensitivity for advanced GC patients.
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         Oncogenes
         Tumour biomarkers
         Life Sciences
         general
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         Cell Biology
         Stem Cells
         Apoptosis
         Cell Cycle Analysis
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