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<p>Thymoma is a mediastinal tumor for which recurrence and therapeutic resistance remain clinical challenges, and cancer stem cell (CSC)-like properties may contribute to these features. This study investigated whether Matrine (Mat) affects stemness-associated features and apoptosis in EL-4-B5 cells and examined the potential involvement of YTHDF1 and Wnt/β-catenin signaling. Mat reduced cell viability and induced apoptosis, with the most evident effects observed at 100&#xa0;µg/mL. Mat also reduced sphere-forming capacity and CD34 expression. Mat treatment decreased YTHDF1 expression and Wnt3a and β-catenin protein levels, whereas YTHDF1 overexpression or LiCl co-treatment partially attenuated these changes. Public-dataset analyses suggested potential clinical relevance of YTHDF1 in thymoma. Because direct m6A measurements, YTHDF1 target identification, in vivo validation, and clinical-sample validation were not performed, these findings support potential involvement of an m6A-related factor and Wnt/β-catenin signaling rather than establishing a definitive mechanism. Further validation is required before translational conclusions can be made.</p>

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Matrine suppresses thymoma stemness and apoptosis via YTH N6-methyladenosine RNA binding protein 1 and Wnt/β-catenin signaling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月15日

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  • Wei Chen,
  • Ruijian Huang,
  • Hongqiang Chen,
  • Ruoxin Yuan,
  • Wu Xue

摘要

Thymoma is a mediastinal tumor for which recurrence and therapeutic resistance remain clinical challenges, and cancer stem cell (CSC)-like properties may contribute to these features. This study investigated whether Matrine (Mat) affects stemness-associated features and apoptosis in EL-4-B5 cells and examined the potential involvement of YTHDF1 and Wnt/β-catenin signaling. Mat reduced cell viability and induced apoptosis, with the most evident effects observed at 100 µg/mL. Mat also reduced sphere-forming capacity and CD34 expression. Mat treatment decreased YTHDF1 expression and Wnt3a and β-catenin protein levels, whereas YTHDF1 overexpression or LiCl co-treatment partially attenuated these changes. Public-dataset analyses suggested potential clinical relevance of YTHDF1 in thymoma. Because direct m6A measurements, YTHDF1 target identification, in vivo validation, and clinical-sample validation were not performed, these findings support potential involvement of an m6A-related factor and Wnt/β-catenin signaling rather than establishing a definitive mechanism. Further validation is required before translational conclusions can be made.