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Updated: Aug 5, 2026

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Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion
Published on: April 2, 2020
Cyr61 Promotes Oral Squamous Cell Carcinoma Cell Motility via an Integrin αvβ3/αvβ5-PLC/PKC/c-Src-AP-1-ICAM-1
Kuan-Chou Lin1,2, Pei-Wen Peng3, Tsung-Ming Chang3
1School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei 110301, Taiwan.
International Journal of Medical Sciences
|July 29, 2026
Summary
Cysteine-rich angiogenic inducer 61 (Cyr61) promotes oral cancer (OSCC) cell migration by upregulating ICAM-1. This study defines a signaling pathway involving integrins, kinases, and AP-1 that drives OSCC metastasis.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Oral squamous cell carcinoma (OSCC) metastasis is a major cause of mortality.
- Cysteine-rich angiogenic inducer 61 (Cyr61/CCN1) is linked to cancer progression, but its role in OSCC cell motility is unclear.
- Elevated Cyr61 expression correlates with advanced OSCC features.
Purpose of the Study:
- To elucidate the downstream molecular mechanisms by which Cyr61 enhances OSCC cell migration.
- To identify key signaling molecules and pathways involved in Cyr61-mediated OSCC motility.
Main Methods:
- OSCC cell lines were treated with recombinant Cyr61.
- Intercellular adhesion molecule-1 (ICAM-1) expression was assessed via mRNA and protein analysis.
- Functional assays (wound closure, Transwell migration) were performed.
- Integrin, kinase, and transcription factor (AP-1) signaling pathways were investigated using antibodies, siRNAs, and pharmacological inhibitors.
Main Results:
- Recombinant Cyr61 increased OSCC cell migration and ICAM-1 expression.
- ICAM-1 silencing reduced Cyr61-induced motility.
- Cyr61 signaling involved integrins αvβ3/αvβ5, PLC, PKC, c-Src, and AP-1.
- Cyr61 enhanced AP-1 activity by phosphorylating c-Jun, leading to increased ICAM-1 promoter occupancy.
Conclusions:
- Cyr61 promotes OSCC cell migration through an integrin-dependent pathway that upregulates ICAM-1 transcriptionally via PLC-PKC-c-Src-AP-1 signaling.
- This study defines a novel Cyr61-driven signaling axis crucial for OSCC metastasis.
- Targeting this pathway may offer therapeutic strategies for OSCC.
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