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<p>Tumor suppressor genes (TSGs) that regulate the stemness of lung cancer cells remain to be determined. We conducted a genome-wide CRISPR/Cas9-mediated screening and identified REPS2 as a potent TSG that negatively regulates the stemness of lung cancer cells. Its tumor suppressive function was confirmed both in vitro and in vivo. Mechanistically, P62 interacts simultaneously with both β-catenin and REPS2, leading to autophagy-lysosome-mediated degradation of β-catenin and attenuation of Wnt signaling. A β-catenin inhibitor synergizes with inhibitors for driver mutants to induce immunogenic cell death, which could be exploited for enhancing efficacy of tumor immunotherapy.</p>

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REPS2 attenuates cancer stemness through inhibiting Wnt signaling by autophagy mediated degradation of β-catenin

  • 期刊论文

  • 发表日期：

    2025年6月13日

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  • Lu Liu,
  • Shuzhen Chen,
  • Yuxi Lei,
  • Zejian Lin,
  • Rulan Zhou,
  • Guandi Zeng,
  • Zongyao Zheng,
  • Wanting Liu,
  • Qian Zhou,
  • Liang Chen

摘要

Tumor suppressor genes (TSGs) that regulate the stemness of lung cancer cells remain to be determined. We conducted a genome-wide CRISPR/Cas9-mediated screening and identified REPS2 as a potent TSG that negatively regulates the stemness of lung cancer cells. Its tumor suppressive function was confirmed both in vitro and in vivo. Mechanistically, P62 interacts simultaneously with both β-catenin and REPS2, leading to autophagy-lysosome-mediated degradation of β-catenin and attenuation of Wnt signaling. A β-catenin inhibitor synergizes with inhibitors for driver mutants to induce immunogenic cell death, which could be exploited for enhancing efficacy of tumor immunotherapy.