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<p>Dysregulation of 5-Hydroxytryptamine and its receptors play important roles in the development and progression of malignant tumors. However, the biological role and underlying molecular mechanism of 5-Hydroxytryptamine Receptor 1D (HTR1D) gastric cancer (GC) remains poorly understood. In this study, we identified that HTR1D was significantly upregulated in GC and can serve as a diagnostic biomarker. High HTR1D expression correlates clinically with poor differentiation and worse prognosis in GC. Gain- and loss-of-function studies demonstrated that HTR1D positively regulated GC cell proliferation, migration, and angiogenesis in vitro and in vivo. RNA sequencing and qRT-PCR assays indicated that HTR1D knockdown significantly inactivated the WNT/β-catenin signaling pathway. Rescue experiments using CHIR-99,021, a known WNT/β-catenin pathway activator, confirmed that HTR1D knockdown inhibited GC invasion by inactivating the WNT/β-catenin pathway. In conclusion, HTR1D overexpression promotes GC progression via activation of the WNT/β-catenin signaling. Our findings highlight HTR1D as an oncogene in GC and suggest that targeting 5-HT1D could serve as a promising therapeutic strategy for GC.</p> Graphical abstract <p></p>

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5-Hydroxytryptamine receptor 1D overexpression exacerbates gastric cancer proliferation, invasion, and angiogenesis by activating the Wnt/β-catenin signaling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月11日

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  • Juan Wu,
  • Yi Yi,
  • Qi Wang,
  • Jinwan Qiao,
  • Haixiu Ma,
  • Jing Zhao,
  • Ronghua Ma,
  • Jun Liu,
  • Haiyan Wang,
  • Zhanhai Su

摘要

Dysregulation of 5-Hydroxytryptamine and its receptors play important roles in the development and progression of malignant tumors. However, the biological role and underlying molecular mechanism of 5-Hydroxytryptamine Receptor 1D (HTR1D) gastric cancer (GC) remains poorly understood. In this study, we identified that HTR1D was significantly upregulated in GC and can serve as a diagnostic biomarker. High HTR1D expression correlates clinically with poor differentiation and worse prognosis in GC. Gain- and loss-of-function studies demonstrated that HTR1D positively regulated GC cell proliferation, migration, and angiogenesis in vitro and in vivo. RNA sequencing and qRT-PCR assays indicated that HTR1D knockdown significantly inactivated the WNT/β-catenin signaling pathway. Rescue experiments using CHIR-99,021, a known WNT/β-catenin pathway activator, confirmed that HTR1D knockdown inhibited GC invasion by inactivating the WNT/β-catenin pathway. In conclusion, HTR1D overexpression promotes GC progression via activation of the WNT/β-catenin signaling. Our findings highlight HTR1D as an oncogene in GC and suggest that targeting 5-HT1D could serve as a promising therapeutic strategy for GC.

Graphical abstract