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Background <p>Colorectal cancer (CRC) is a major global health issue, characterized by high incidence and mortality rates. This study aims to further elucidate the function of H domain of Fc fragment of IgG binding protein (HFCGBP), as a candidate tumor suppressor gene, in the progression of CRC and its clinical implications.</p> Methods <p>A comprehensive methodological approach was employed, encompassing the collection of clinical samples, proliferation and migration assays, immunohistochemistry, and in-depth data analysis.</p> Results <p>The downregulation of FCGBP expression was significant negatively correlated with tumor stage and grade in CRC tissues. Importantly, the overexpression of HFCGBP in CRC cells resulted in a notable inhibition of cell proliferation and migration, highlighting its potential as a therapeutic target. Combined with bioinformatic analysis of RNA-seq, the key signaling pathways modulated by HFCGBP, such as neuroactive ligand-receptor interaction and platelet activation, were identified, thereby offering valuable insights into its regulatory mechanisms. Furthermore, the analysis of TCGA and Gene Expression Omnibus (GEO) databases further confirmed the reduced expression of FCGBP in various tumor types, with a particular focus on CRC, reinforcing its potential as a prognostic biomarker. It underscores the crucial role of HFCGBP in CRC and its promising potential as a therapeutic target.</p>

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The tumor-suppressive function of the unique H domain of FCGBP and its potential as a therapeutic target in colorectal cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月16日

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  • Qiao Liu,
  • Hong-ying Jiao,
  • Yuan-yuan Wang,
  • Liao-liao Zhu,
  • Ni Wang,
  • Chong Liu,
  • Jing Tian,
  • Qian-nan Wang,
  • Yang Li,
  • Wei Zhang,
  • Na Ning,
  • Li Gong

摘要

Background

Colorectal cancer (CRC) is a major global health issue, characterized by high incidence and mortality rates. This study aims to further elucidate the function of H domain of Fc fragment of IgG binding protein (HFCGBP), as a candidate tumor suppressor gene, in the progression of CRC and its clinical implications.

Methods

A comprehensive methodological approach was employed, encompassing the collection of clinical samples, proliferation and migration assays, immunohistochemistry, and in-depth data analysis.

Results

The downregulation of FCGBP expression was significant negatively correlated with tumor stage and grade in CRC tissues. Importantly, the overexpression of HFCGBP in CRC cells resulted in a notable inhibition of cell proliferation and migration, highlighting its potential as a therapeutic target. Combined with bioinformatic analysis of RNA-seq, the key signaling pathways modulated by HFCGBP, such as neuroactive ligand-receptor interaction and platelet activation, were identified, thereby offering valuable insights into its regulatory mechanisms. Furthermore, the analysis of TCGA and Gene Expression Omnibus (GEO) databases further confirmed the reduced expression of FCGBP in various tumor types, with a particular focus on CRC, reinforcing its potential as a prognostic biomarker. It underscores the crucial role of HFCGBP in CRC and its promising potential as a therapeutic target.