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<p>Bufalin, a main active monomer component extracted from the Traditional Chinese Medicine toad venom, exhibits potent anti-tumour activity across diverse malignancies. However, its specific molecular targets in Oesophageal squamous cell carcinoma (ESCC) remain unclear. Here, we demonstrate that bufalin suppresses ESCC growth and metastasis in a concentration-dependent manner both in vitro and in vivo. RNA sequencing analysis revealed that bufalin inhibits ESCC progression by downregulating LINC01410. TCGA-ESCC data indicated that LINC01410 is highly expressed in ESCC tissues and promotes tumour progression by stabilising β-catenin protein and activating the Wnt/β-catenin pathway. Through multiple approaches including proteome microarray screening and machine learning analyses, we identified E2F2 as a upstream transcription factor of LINC01410. We further demonstrate that bufalin induces the proteasomal degradation of E2F2, consequently silencing LINC01410 transcription and collapsing the LINC01410-Wnt/β-catenin signalling axis. In summary, our findings indicate that bufalin targets E2F2 to downregulate LINC01410, thereby providing a potential therapeutic strategy for suppressing ESCC progression.</p>

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Bufalin targets E2F2 to transcriptionally inhibit LINC01410 and suppress Wnt/β-catenin signaling in esophageal squamous cell carcinoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月18日

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  • Xiaohong Kang,
  • Yufei Ma,
  • Hongke Zhao,
  • Haoling Zhang,
  • Mridul Roy,
  • Mingjuan Liao,
  • Ying Wei,
  • Xingqiao Li,
  • Yueyang Zhou,
  • Huange Xue,
  • Xiaoxia Yan,
  • Wangzheqi Zhang,
  • Yadong Guo,
  • Fei Cao,
  • Tingmin Chang

摘要

Bufalin, a main active monomer component extracted from the Traditional Chinese Medicine toad venom, exhibits potent anti-tumour activity across diverse malignancies. However, its specific molecular targets in Oesophageal squamous cell carcinoma (ESCC) remain unclear. Here, we demonstrate that bufalin suppresses ESCC growth and metastasis in a concentration-dependent manner both in vitro and in vivo. RNA sequencing analysis revealed that bufalin inhibits ESCC progression by downregulating LINC01410. TCGA-ESCC data indicated that LINC01410 is highly expressed in ESCC tissues and promotes tumour progression by stabilising β-catenin protein and activating the Wnt/β-catenin pathway. Through multiple approaches including proteome microarray screening and machine learning analyses, we identified E2F2 as a upstream transcription factor of LINC01410. We further demonstrate that bufalin induces the proteasomal degradation of E2F2, consequently silencing LINC01410 transcription and collapsing the LINC01410-Wnt/β-catenin signalling axis. In summary, our findings indicate that bufalin targets E2F2 to downregulate LINC01410, thereby providing a potential therapeutic strategy for suppressing ESCC progression.