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Background <p>Esophageal squamous cell carcinoma (ESCC) represents a highly lethal malignancy. The FOXA2 was involved in cellular proliferation, differentiation, tumorigenesis, and metastasis. The precise regulatory mechanisms of FOXA2 in ESCC progression remain unclear.</p> Materials and methods <p>Western blotting, reverse transcription-quantitative polymerase chain reaction, and immunohistochemistry were used to detect the expression level of FOXA2, CCK-8, transwell, and wound healing assays in vitro and xenograft tumor model in vivo were applied to assess the function of FOXA2. RNA-Seq analysis and the following functional assays were used to elucidate the relationship between FOXA2 and proteasome activity.</p> Results <p>The expression level of FOXA2 was downregulated in ECSS tissues and cells. Overexpression of FOXA2 in ESCC cells inhibited epithelial-mesenchymal transition in ESCC cells with the upregulation of E-cadherin and downregulation of Vimentin. Meanwhile, overexpression of FOXA2 inhibited the proliferation, migration, and invasion of ESCC cells. Mechanically, proteasome was involved in the ESCC cells proliferation and invasion inhibition induced by FOXA2, and reduced proteasome activity inhibited ESCC cells proliferation and invasion. RNA-Seq analysis identified PSMB9 as a key downstream target, indicating that FOXA2 attenuates proteasome activity by suppressing PSMB9 expression.</p> Conclusion <p>FOXA2 suppresses ESCC proliferation and invasion by modulating proteasome activity through PSMB9, highlighting its critical role in ESCC progression and its potential as a therapeutic target.</p>

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FOXA2 suppresses ESCC proliferation and metastasis by inhibiting PSMB9 expression, thereby attenuating proteasome activity

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月17日

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  • Wenqiang Xia,
  • Ning Li,
  • Chunxia Gong,
  • Xin Li,
  • Hao Li,
  • Bowen Shi,
  • Hezhong Chen

摘要

Background

Esophageal squamous cell carcinoma (ESCC) represents a highly lethal malignancy. The FOXA2 was involved in cellular proliferation, differentiation, tumorigenesis, and metastasis. The precise regulatory mechanisms of FOXA2 in ESCC progression remain unclear.

Materials and methods

Western blotting, reverse transcription-quantitative polymerase chain reaction, and immunohistochemistry were used to detect the expression level of FOXA2, CCK-8, transwell, and wound healing assays in vitro and xenograft tumor model in vivo were applied to assess the function of FOXA2. RNA-Seq analysis and the following functional assays were used to elucidate the relationship between FOXA2 and proteasome activity.

Results

The expression level of FOXA2 was downregulated in ECSS tissues and cells. Overexpression of FOXA2 in ESCC cells inhibited epithelial-mesenchymal transition in ESCC cells with the upregulation of E-cadherin and downregulation of Vimentin. Meanwhile, overexpression of FOXA2 inhibited the proliferation, migration, and invasion of ESCC cells. Mechanically, proteasome was involved in the ESCC cells proliferation and invasion inhibition induced by FOXA2, and reduced proteasome activity inhibited ESCC cells proliferation and invasion. RNA-Seq analysis identified PSMB9 as a key downstream target, indicating that FOXA2 attenuates proteasome activity by suppressing PSMB9 expression.

Conclusion

FOXA2 suppresses ESCC proliferation and invasion by modulating proteasome activity through PSMB9, highlighting its critical role in ESCC progression and its potential as a therapeutic target.