Integrin β5 interacts with G3BP1 through activating FAK/Src signaling pathway to promote gastric carcinogenesis

Previous studies demonstrated that integrin β5 (ITGB5) play an important role in the occurrence and development of various malignant tumors. However, its functional mechanism in gastric cancer (GC) remains obscure. We detected that ITGB5 was overexpressed in GC tissues and its high-level expression...

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Vydané v:Scientific reports Ročník 15; číslo 1; s. 28633 - 13
Hlavní autori: Liu, Dongliang, Cao, Jianjian, Hu, Kongwang, Peng, Zhiwei
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: London Nature Publishing Group UK 05.08.2025
Nature Publishing Group
Nature Portfolio
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Binding sites
Cancer therapies
Carcinogenesis
Cell growth
Cell proliferation
Chemical bonds
Efficiency
FAK/Src signaling
Focal adhesion kinase
G3BP1
Gastric cancer
Gastric carcinogenesis
Humanities and Social Sciences
Integrin β5
Invasion
Invasiveness
Kinases
Ligands
Medical prognosis
Metastasis
multidisciplinary
Pancreatic cancer
Phosphorylation
Protein expression
Proteins
Science
Science (multidisciplinary)
Signal transduction
Therapeutic targets
Tumorigenesis
Wound healing
Gastric carcinogenesis
FAK/Src signaling
Integrin β5
Invasion
G3BP1
ISSN:2045-2322, 2045-2322
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Shrnutí:Previous studies demonstrated that integrin β5 (ITGB5) play an important role in the occurrence and development of various malignant tumors. However, its functional mechanism in gastric cancer (GC) remains obscure. We detected that ITGB5 was overexpressed in GC tissues and its high-level expression was associated with poor survival and advanced stages. Functional assays indicated that overexpression of ITGB5 promotes the proliferation, migration and invasion of GC cells in both vitro and vivo. Mechanistically, we observed a lower variability and invasiveness when GC cells were treated with Defactinib and Saractinib, indicating that activated FAK-Src signaling may lead to an aggressive GC process. Then, we reveal that knockdown of ITGB5 reduces phosphorylation of FAK and Src, without changing total FAK/Src levels. Additionally, ITGB5 interacts with G3BP1 and increases the phosphorylation of FAK and Src. This leads to activation of FAK/Src signaling, which are critical regulators of GC development. Our findings uncover a previously unrecognized mechanism of the ITGB5/G3BP1/FAK/Src axis involved in GC development and the oncogenic potential of ITGB5 in GC, thus providing a potential therapeutic target for advanced GC.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:2045-2322
2045-2322
DOI:10.1038/s41598-025-14067-z