Fc fragment of IgG binding protein suppresses tumor growth by stabilizing wild type P53 in colorectal cancer cells.

IF 3.4 2区 医学 Q2 ONCOLOGY BMC Cancer Pub Date : 2025-03-19 DOI:10.1186/s12885-025-13873-y
Jiefu Wang, Ziqing Gong, Jia Liu, Wenpeng Wang, Kai Liu, Yanpeng Yang, Xinran Lu, Junfeng Wang
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Abstract

The Fc fragment of IgG binding protein (FCGBP) exhibits differential expression across various tumor types. but its role in cancer progression remains underexplored. This research discovered that FCGBP is downregulated in colorectal cancer (CRC) cells and is negatively associated with poor prognosis. Overexpression of FCGBP inhibited the growth of P53 wild-type CRC cells both in vitro and in vivo. Mechanistically, immunoprecipitation experiments revealed that FCGBP competitively binds to MDM2, thereby attenuating the formation of the P53/MDM2 complex. This, in turn, reduces P53 ubiquitination and stabilizes the protein. Our findings reveal a novel mechanism through which FCGBP significantly inhibits CRC cell growth and propose a new targeted therapeutic strategy for CRC treatment.

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IgG结合蛋白Fc片段通过稳定野生型P53抑制结直肠癌细胞的肿瘤生长。
IgG结合蛋白Fc片段(FCGBP)在不同肿瘤类型中表现出差异表达。但它在癌症进展中的作用仍未得到充分研究。本研究发现,FCGBP在结直肠癌(CRC)细胞中下调,与预后不良呈负相关。在体外和体内实验中,过表达FCGBP可抑制P53野生型CRC细胞的生长。机制上,免疫沉淀实验显示FCGBP与MDM2竞争性结合,从而减弱P53/MDM2复合物的形成。反过来,这减少了P53的泛素化并稳定了蛋白质。我们的研究结果揭示了FCGBP显著抑制结直肠癌细胞生长的新机制,并为结直肠癌治疗提供了新的靶向治疗策略。
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索莱宝
crystal violet
来源期刊
BMC Cancer
BMC Cancer 医学-肿瘤学
CiteScore
6.00
自引率
2.60%
发文量
1204
审稿时长
6.8 months
期刊介绍: BMC Cancer is an open access, peer-reviewed journal that considers articles on all aspects of cancer research, including the pathophysiology, prevention, diagnosis and treatment of cancers. The journal welcomes submissions concerning molecular and cellular biology, genetics, epidemiology, and clinical trials.
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