ArticleAmerican journal of translational research2026
FCGBP promotes malignant phenotypes of glioblastoma cells via activation of the TGF-β1 signaling pathway.
Article in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo investigate the expression level of IgG Fc-binding protein (FCGBP) in glioma cells, elucidate its role in malignant tumor phenotypes, and explore its relationship with the transforming growth factor-β (TGF-β) signaling pathway.
methodsThe expression of FCGBP was compared between primary human astrocytes (HA) and glioma cell lines (U87, U251, LN229, and T98G). FCGBP was then silenced in U87 cells. Cell proliferation, migration, and invasion were assessed using Cell Counting Kit-8, 5-ethynyl-2'-deoxyuridine (EdU) incorporation, colony formation, wound healing, and Matrigel-coated Transwell assays. Apoptosis and cell-cycle distribution in U87 cells were analyzed by flow cytometry. Co-immunoprecipitation (Co-IP) was performed to validate the endogenous association between FCGBP and TGF-β1-containing protein complexes. Rescue experiments were conducted using recombinant TGF-β1 protein. Additionally, the in vitro findings were further validated in nude mouse xenograft models.
resultsFCGBP was highly expressed in various glioma cell lines, and its knockdown reduced TGF-β levels in the culture supernatant. Knockdown of FCGBP in U87 cells significantly suppressed malignant behaviors, including proliferation, migration, and invasion, while inducing apoptosis and cell-cycle arrest. Co-IP assays suggested an endogenous association between FCGBP and TGF-β1-containing protein complexes, and treatment with recombinant TGF-β1 effectively reversed the inhibitory effects of FCGBP knockdown.
conclusionFCGBP promotes malignant phenotypes in glioma cells (U87) and accelerates tumor growth
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