ArticleBMC cancer2025
Unveiling the ITGβ1-CLIC1 axis: a new frontier in oral squamous cell carcinoma progression and immune evasion: insights from the tumor-mimetic ECM system.
Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Designing the matrix: extracellular matrix-informed strategies for bioengineered cancer models.Frontiers in bioengineering and biotechnology · 2026Review
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Abstract
backgroundThe progression of oral squamous cell carcinoma (OSCC) is critically influenced by the dynamic interaction between the tumor and immunosuppressive microenvironment. Integrin β1 (ITGβ1, ITGB1), a pivotal mediator of cell-extracellular matrix (ECM) interaction, not only facilitates tumor invasion but may also plays a role in immune evasion, which remains inadequately understood. Emerging evidence indicates that ITGβ1 collaborates with chloride intracellular channel 1 (CLIC1) to regulate both the ECM remodeling and immunological function. This study examines the ITGβ1-CLIC1 axis in OSCC progression and its potential role in shaping the tumor immune landscape.
methodsThe Gene Expression Omnibus (GEO) and Tumor Immune Estimation Resource (TIMER) databases were analyzed to evaluate ITGβ1 expression and its potential interaction partners in OSCC, with particular attention to tumor immune infiltration. Clinical tissues and associated data were gathered to assess the expression of ITGβ1 and CLIC1, and the relevance in a clinical context. To investigate the ECM-mediated regulation of ITGβ1 signaling, the tumor-mimetic ECM system was developed to replicate the native architecture of the tumor ECM and its immune-modulatory components. The system facilitated to investigate influences of ECM-ITGβ1 on OSCC cell migration, proliferation, and invasion. Additionally, to elucidate the interaction between ITGβ1 and CLIC1, western blot analysis of CLIC1 expression following ITGβ1 inhibition was conducted.
resultsAnalysis of the GEO database revealed that ITGβ1 is upregulated in OSCC and interacted with CLIC1. Further investigation utilizing TIMER2.0 analysis to examine the correlations between ITGβ1 and CLIC1 and the infiltration of specific immune cells, such as T follicular helper cells, suggesting a potential immune evasion. The expression levels of ITGβ1 and CLIC1 were significantly elevated in OSCC compared to the normal tissues, correlated with a poorer prognosis. In the tumor-mimetic ECM system, ITGβ1 overexpression was associated with enhanced proliferation, migration, and invasion of OSCC cells, indicating its potential role in ECM-regulated tumor behaviors. Subsequent western blot analysis identified a co-expression pattern between ITGβ1 and CLIC1.
conclusionThis study provides evidence supporting the association between the ITGβ1-CLIC1 axis and OSCC progression, and suggests its potential involvement in modulating the tumor immune microenvironment, indicating its promise as a therapeutic target worthy of further investigation.
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