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Updated: Jun 13, 2026

Preparation of Naringenin Solution for In Vivo Application
Published on: August 10, 2021
Naringenin, a Food-Derived Flavanone, Suppresses ITGA11-Associated Gastric Cancer Progression via the
Qiang Li1, Guiyang Ye1, Fangfang Chen2
1Department of Gastrointestinal Surgery I Section, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Abstract:
(1) Background: Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide. Aberrant remodeling of the extracellular matrix (ECM) is a hallmark of GC progression; however, the mechanisms by which GC cells sense and exploit ECM cues remain unclear. (2) Methods: ITGA11 was identified through integrative bioinformatic analyses. Its expression, clinical significance, and association with ECM-related signatures were evaluated in GC tissues and public datasets. The function of ITGA11 and its role in regulating the FAK/PI3K/AKT/mTOR pathway were investigated using in vitro and in vivo assays, and the inhibitory effect of Naringenin on ITGA11-associated oncogenic activity was assessed. (3) Results: ITGA11 was upregulated in GC tissues and correlated with an ECM-related gene signature, aggressive clinicopathological features and poor patient survival. ITGA11 promoted malignant phenotypes of GC cells in vitro and in vivo. Importantly, molecular docking and target engagement assays suggested a potential interaction between Naringenin and ITGA11. Functional experiments showed that Naringenin attenuated ITGA11-associated oncogenic activity by reducing ITGA11 levels, suppressing pathway activation, and inhibiting malignant phenotypes. (4) Conclusions: Our findings identify ITGA11 as a potential prognostic biomarker and functional driver of GC progression and suggest that Naringenin may represent a promising bioactive compound for modulating the ITGA11/FAK/PI3K/AKT/mTOR axis in GC.
Insights
Integrin alpha-11 (ITGA11) drives gastric cancer (GC) progression by altering the extracellular matrix. The compound Naringenin effectively inhibits ITGA11 activity, offering a potential therapeutic strategy for GC.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Gastric cancer (GC) is a major global health concern, with poor outcomes often linked to extracellular matrix (ECM) dysregulation.
- The precise mechanisms by which GC cells interact with and are influenced by the ECM are not fully understood.
- Aberrant ECM remodeling is a critical factor in GC progression.
Purpose of the Study:
- To investigate the role of Integrin alpha-11 (ITGA11) in GC progression.
- To explore the association between ITGA11 expression and clinical outcomes in GC patients.
- To assess the potential of Naringenin as a therapeutic agent targeting the ITGA11 pathway in GC.
Main Methods:
- Integrative bioinformatics analyses were used to identify ITGA11.
- ITGA11 expression, clinical significance, and ECM associations were evaluated in GC tissues and public datasets.
- In vitro and in vivo assays examined ITGA11 function and its regulation of the FAK/PI3K/AKT/mTOR pathway. Naringenin's inhibitory effects were assessed.
Main Results:
- ITGA11 was found to be upregulated in GC tissues, correlating with aggressive features and poor survival.
- ITGA11 promoted malignant phenotypes in GC cells both in vitro and in vivo.
- Naringenin demonstrated potential interaction with ITGA11, reducing its levels, suppressing pathway activation, and inhibiting GC cell malignancy.
Conclusions:
- ITGA11 serves as a potential prognostic biomarker and functional driver in gastric cancer.
- Naringenin shows promise as a bioactive compound for targeting the ITGA11/FAK/PI3K/AKT/mTOR axis in GC therapy.
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