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. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12885-026-15718-8.
The tumor-suppressive function of the unique H domain of FCGBP and its potential as a therapeutic target in colorectal cancer.
阅读:2
作者:Liu Qiao, Jiao Hong-Ying, Wang Yuan-Yuan, Zhu Liao-Liao, Wang Ni, Liu Chong, Tian Jing, Wang Qian-Nan, Li Yang, Zhang Wei, Ning Na, Gong Li
| 期刊: | BMC Cancer | 影响因子: | 3.400 |
| 时间: | 2026 | 起止号: | 2026 Feb 16; 26(1):450 |
| doi: | 10.1186/s12885-026-15718-8 | ||
特别声明
1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。
2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。
3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。
4、投稿及合作请联系:info@biocloudy.com。
