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<p>PANoptosis is an inflammatory programmed cell death mechanism that depends on the PANoptosome complex, which integrates hallmark features of apoptosis, necroptosis, and pyroptosis. Meiotic nuclear division protein 1 (MND1), a meiosis-specific protein, primarily participates in homologous chromosome pairing and DNA double-strand break repair. However, the precise role of MND1 in regulating PANoptosis and tumor stemness remains unclear. Here, we provide evidence that MND1 participates in the regulatory mechanisms of PANoptosis and cell stemness in lung adenocarcinoma (LUAD). Mechanistically, MND1 recruits PABPC1 to interact with the 3’-UTR of RCOR2 mRNA, significantly enhancing its stability. As a crucial component of the pluripotency regulatory network, the stable expression of RCOR2 is essential for maintaining tumor cell stemness. Our findings suggest MND1 acts as an oncogene in LUAD by stabilizing RCOR2 mRNA, maintaining the stemness of LUAD and inhibiting PANoptosis. Notably, this study represents the first investigation to elucidate the regulatory role of MND1 in modulating both stemness properties and PANoptosis in LUAD, providing valuable insights into the molecular mechanisms underlying LUAD pathogenesis.</p>

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MND1 regulates PANoptosis and stemness of lung adenocarcinoma cells by stabilizing RCOR2 mRNA

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月10日

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  • Lianlian Ouyang,
  • Xingjie Tang,
  • Shiyao Jiang,
  • Yating Liu,
  • Na Liu,
  • Chao Mao,
  • Yuanbing Chen,
  • Ye Fan,
  • Ziyun Zhang,
  • Jingjing Huang,
  • Yongguang Tao,
  • Xing Yu,
  • Li Cong,
  • Yiqun Jiang

摘要

PANoptosis is an inflammatory programmed cell death mechanism that depends on the PANoptosome complex, which integrates hallmark features of apoptosis, necroptosis, and pyroptosis. Meiotic nuclear division protein 1 (MND1), a meiosis-specific protein, primarily participates in homologous chromosome pairing and DNA double-strand break repair. However, the precise role of MND1 in regulating PANoptosis and tumor stemness remains unclear. Here, we provide evidence that MND1 participates in the regulatory mechanisms of PANoptosis and cell stemness in lung adenocarcinoma (LUAD). Mechanistically, MND1 recruits PABPC1 to interact with the 3’-UTR of RCOR2 mRNA, significantly enhancing its stability. As a crucial component of the pluripotency regulatory network, the stable expression of RCOR2 is essential for maintaining tumor cell stemness. Our findings suggest MND1 acts as an oncogene in LUAD by stabilizing RCOR2 mRNA, maintaining the stemness of LUAD and inhibiting PANoptosis. Notably, this study represents the first investigation to elucidate the regulatory role of MND1 in modulating both stemness properties and PANoptosis in LUAD, providing valuable insights into the molecular mechanisms underlying LUAD pathogenesis.