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<p>Gliomas are highly aggressive brain tumors with complex molecular characteristics. The role of BEX1 methylation in gliomas is not well understood, despite its potential implications for tumor biology and therapy. Investigating this relationship could uncover critical mechanisms underlying glioma pathogenesis and highlight therapeutic targets. This study aims to elucidate the specific mechanisms by which BEX1 methylation regulates the cell cycle and apoptosis in glioma. We conducted bioinformatics analyses to assess BEX1 expression differences in glioma using tissue samples, followed by validation through Western blot and qRT-PCR. Functional assays in glioma cell lines were performed, employing gene transfection and small molecule inhibitors to further explore BEX1’s role in the AKT/ERK/STAT3 signaling pathways. Our findings reveal that BEX1 is significantly downregulated in gliomas due to promoter methylation, which in turn activates the AKT/ERK/STAT3 signaling cascade, leading to alterations in cell cycle regulation and apoptosis. Targeting BEX1 methylation presents a promising therapeutic avenue for glioma treatment. This study provides valuable insights into the mechanisms of BEX1 in glioma, paving the way for clinical translation and further research. </p>

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RETRACTED ARTICLE: Methylation-induced suppression of BEX1 activates AKT/ERK/STAT3 signaling pathways regulating cell cycle and apoptosis in glioma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年8月13日

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  • Li-Zhi Xiao,
  • Shi Feng ,
  • Zhen He,
  • Rui Mao,
  • Kai Qian,
  • Zhi-Ying Zhou,
  • Huabao Cai,
  • Mengyu Zhao,
  • Cunzhi Wang,
  • Tianhang Yu,
  • Zi-Yu Zhao,
  • Jie Li

摘要

Gliomas are highly aggressive brain tumors with complex molecular characteristics. The role of BEX1 methylation in gliomas is not well understood, despite its potential implications for tumor biology and therapy. Investigating this relationship could uncover critical mechanisms underlying glioma pathogenesis and highlight therapeutic targets. This study aims to elucidate the specific mechanisms by which BEX1 methylation regulates the cell cycle and apoptosis in glioma. We conducted bioinformatics analyses to assess BEX1 expression differences in glioma using tissue samples, followed by validation through Western blot and qRT-PCR. Functional assays in glioma cell lines were performed, employing gene transfection and small molecule inhibitors to further explore BEX1’s role in the AKT/ERK/STAT3 signaling pathways. Our findings reveal that BEX1 is significantly downregulated in gliomas due to promoter methylation, which in turn activates the AKT/ERK/STAT3 signaling cascade, leading to alterations in cell cycle regulation and apoptosis. Targeting BEX1 methylation presents a promising therapeutic avenue for glioma treatment. This study provides valuable insights into the mechanisms of BEX1 in glioma, paving the way for clinical translation and further research.