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

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...

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Main Authors: Jiefu Wang, Ziqing Gong, Jia Liu, Wenpeng Wang, Kai Liu, Yanpeng Yang, Xinran Lu, Junfeng Wang
Format: Article
Language:English
Published: BMC 2025-03-01
Series:BMC Cancer
Subjects:
Online Access:https://doi.org/10.1186/s12885-025-13873-y
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author Jiefu Wang
Ziqing Gong
Jia Liu
Wenpeng Wang
Kai Liu
Yanpeng Yang
Xinran Lu
Junfeng Wang
author_facet Jiefu Wang
Ziqing Gong
Jia Liu
Wenpeng Wang
Kai Liu
Yanpeng Yang
Xinran Lu
Junfeng Wang
author_sort Jiefu Wang
collection DOAJ
description 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.
format Article
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institution DOAJ
issn 1471-2407
language English
publishDate 2025-03-01
publisher BMC
record_format Article
series BMC Cancer
spelling doaj-art-174d5ec49542495c849d559a94765fb72025-08-20T02:41:32ZengBMCBMC Cancer1471-24072025-03-012511910.1186/s12885-025-13873-yFc fragment of IgG binding protein suppresses tumor growth by stabilizing wild type P53 in colorectal cancer cellsJiefu Wang0Ziqing Gong1Jia Liu2Wenpeng Wang3Kai Liu4Yanpeng Yang5Xinran Lu6Junfeng Wang7Tianjin’s Clinical Research Center for Cancer, Tianjin Key Laboratory of Digestive Cancer, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for CancerTianjin’s Clinical Research Center for Cancer, Tianjin Key Laboratory of Digestive Cancer, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for CancerTianjin’s Clinical Research Center for Cancer, Tianjin Key Laboratory of Digestive Cancer, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for CancerTianjin’s Clinical Research Center for Cancer, Tianjin Key Laboratory of Digestive Cancer, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for CancerTianjin’s Clinical Research Center for Cancer, Tianjin Key Laboratory of Digestive Cancer, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for CancerTianjin’s Clinical Research Center for Cancer, Tianjin Key Laboratory of Digestive Cancer, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for CancerPeking University Health Science CenterTianjin’s Clinical Research Center for Cancer, Tianjin Key Laboratory of Digestive Cancer, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for CancerAbstract 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.https://doi.org/10.1186/s12885-025-13873-yFc fragment of IgG binding proteinColorectal cancerWild type P53UbiquitinationMDM2
spellingShingle Jiefu Wang
Ziqing Gong
Jia Liu
Wenpeng Wang
Kai Liu
Yanpeng Yang
Xinran Lu
Junfeng Wang
Fc fragment of IgG binding protein suppresses tumor growth by stabilizing wild type P53 in colorectal cancer cells
BMC Cancer
Fc fragment of IgG binding protein
Colorectal cancer
Wild type P53
Ubiquitination
MDM2
title Fc fragment of IgG binding protein suppresses tumor growth by stabilizing wild type P53 in colorectal cancer cells
title_full Fc fragment of IgG binding protein suppresses tumor growth by stabilizing wild type P53 in colorectal cancer cells
title_fullStr Fc fragment of IgG binding protein suppresses tumor growth by stabilizing wild type P53 in colorectal cancer cells
title_full_unstemmed Fc fragment of IgG binding protein suppresses tumor growth by stabilizing wild type P53 in colorectal cancer cells
title_short Fc fragment of IgG binding protein suppresses tumor growth by stabilizing wild type P53 in colorectal cancer cells
title_sort fc fragment of igg binding protein suppresses tumor growth by stabilizing wild type p53 in colorectal cancer cells
topic Fc fragment of IgG binding protein
Colorectal cancer
Wild type P53
Ubiquitination
MDM2
url https://doi.org/10.1186/s12885-025-13873-y
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