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Purpose <p>Trophinin-associated protein (TROAP) plays a crucial role in various human cancers. However, its involvement in esophageal squamous cell carcinoma (ESCC) remains unclear. This study aimed to explore the clinical significance and biological function of TROAP in ESCC.</p> Methods <p>The expression and clinical relevance of TROAP in ESCC were analyze using GEO and TCGA databases. TROAP expression in ESCC samples was further validated by qRT-PCR, western blotting, and immunohistochemistry. In vitro and in vivo experiments were performed to assess TROAP’s role in ESCC progression. RNA-seq analysis followed by western blotting and pathway-specific activator were conducted to explore the underlying mechanism.</p> Results <p>TROAP was found to be overexpressed in ESCC and was positively correlated with higher histological grade and advanced clinical stage. Overexpression of TROAP promoted the proliferation, migration, and invasion of ESCC cells in vitro, whereas knockdown of TROAP suppressed ESCC progression both in vitro and in vivo. Mechanistically, TROAP facilitated ESCC progression by activating PI3K/AKT signaling pathway.</p> Conclusion <p>This study revealed that TROAP promotes ESCC progression via activating PI3K/AKT pathway, suggesting that TROAP might be a promising therapeutic target for ESCC.</p>

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TROAP promotes esophageal squamous cell carcinoma progression via the PI3K/AKT pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月19日

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  • Liqiang Shi,
  • Yajie Zhang,
  • Cong Yang,
  • Yaxin Wang,
  • Yichao Han,
  • Chuanyin Li,
  • Yun Yang,
  • Dong Dong,
  • Mingyuan Du,
  • Hecheng Li

摘要

Purpose

Trophinin-associated protein (TROAP) plays a crucial role in various human cancers. However, its involvement in esophageal squamous cell carcinoma (ESCC) remains unclear. This study aimed to explore the clinical significance and biological function of TROAP in ESCC.

Methods

The expression and clinical relevance of TROAP in ESCC were analyze using GEO and TCGA databases. TROAP expression in ESCC samples was further validated by qRT-PCR, western blotting, and immunohistochemistry. In vitro and in vivo experiments were performed to assess TROAP’s role in ESCC progression. RNA-seq analysis followed by western blotting and pathway-specific activator were conducted to explore the underlying mechanism.

Results

TROAP was found to be overexpressed in ESCC and was positively correlated with higher histological grade and advanced clinical stage. Overexpression of TROAP promoted the proliferation, migration, and invasion of ESCC cells in vitro, whereas knockdown of TROAP suppressed ESCC progression both in vitro and in vivo. Mechanistically, TROAP facilitated ESCC progression by activating PI3K/AKT signaling pathway.

Conclusion

This study revealed that TROAP promotes ESCC progression via activating PI3K/AKT pathway, suggesting that TROAP might be a promising therapeutic target for ESCC.