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Cysteine-Rich 61 (CCN1) Enhances Chemotactic Migration, Transendothelial Cell Migration, and Intravasation by Concomitantly Up-Regulating Chemokine Receptor 1 and 2
Open accessAbstract
Cysteine-rich 61 (Cyr61; CCN1) plays an important role in tumor development and progression in many kinds of human malignancies. Here, we further show the enforced expression of the Cyr61 gene or treatment with recombinant Cyr61 protein enhanced expression of chemokine receptors CXCR1 and CXCR2 in gastric cancer AGS cells. Attenuation of Cyr61 levels in MKN-45 cells by transfecting with antisense Cyr61 significantly reduced the level of CXCR1 and CXCR2. It is suggested that Cyr61 tightly regulates the downstream genes CXCR1 and CXCR2 in gastric cancer cells. Supportively, reverse transcription–PCR and immunohistochemical analysis of human gastric adenocarcinoma showed that there was a high correlation between the expression level of Cyr61 and CXCR1/CXCR2. The up-regulated functionality of CXCR1 andCXCR2 in Cyr61-overexpressing AGS cells could facilitate their chemotactic migration toward interleukin-8, a physiologic ligand of CXCR1 and CXCR2. In addition, the Cyr61-mediated up-regulation of CXCR1/CXCR2 also contributed to transendothelial migration, as well as intravasation in a chick embryo model. Pharmacologic and genetic approaches revealed that phosphoinositide 3-kinase (PI3K)/Akt, but not extracellular signal-regulated kinase 1/2 or p38, signaling pathway is requisite for the up-regulation of CXCR1/CXCR2 mRNA and protein induced by Cyr61. Function-neutralizing antibody to integrin αvβ3, but not α2β1, effectively abolished Cyr61-elicited Src activation and the subsequent PI3K/Akt pathway. Antagonists toward integrin αvβ3, Src kinase, and PI3K/Akt not only suppressed CXCR1/CXCR2 elevation but also blocked chemotactic migration induced by Cyr61. In conclusion, we suggest that Cyr61 promotes interleukin-8–dependent chemotaxis, transendothelial migration, and intravasation by induction of CXCR1/CXCR2 through integrin αvβ3/Src/PI3K/Akt–dependent pathway. (Mol Cancer Res 2007;5(11):1111–23)
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CCN1 stimulates cell migration in fibroblasts, smooth muscle cells, endothelial cells, and certain cancer cells.
“Furthermore, CCN1 stimulates cell migration in fibroblasts, smooth muscle cells and endothelial cells [56,71,72], and certain cancer cells [73–75].”
From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [73]
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References 64 · Cited by 51
Metadata
- Authors
- Lin, B.-R., Chang, C.-C., Chen, L.-R., Wu, M.-H., Wang, M.-Y., Kuo, I.-H., Chu, C.-Y., Chang, K.-J., Lee, P.-H., Chen, W.-J., Kuo, M.-L., & Lin, M.-T.
- Affiliations
- 1Department of Surgery,
- 2Laboratory of Molecular and Cellular Toxicology, Institute of Toxicology, College of Medicine,
- National Taiwan University (TW)
- ORCID
- Venue
- Molecular Cancer Research
- Published
- 2007-11-01
- Volume
- 5
- Issue
- 11
- Pages
- 1111-1123
- ISSN
- 1541-7786 (ISSN-L)
- 1557-3125
- OpenAlex
- W2146133427
- Cited by
- 51
- References
- 64
- Citations by year
- 2025: 1 · 2024: 3 · 2023: 1 · 2022: 1 · 2021: 4 · 2020: 2 · 2018: 4 · 2016: 5 · 2015: 6 · 2014: 4 · 2013: 5 · 2012: 4
- FWCI
- 1.05
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Science Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connective Tissue Growth Factor Research
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
- Keywords
- CYR61, CXCR1, CXCR2, gastric cancer, chemotactic migration, transendothelial migration, intravasation, interleukin-8, integrin αvβ3, Src kinase, PI3K/Akt signaling, metastasis
- MeSH terms
- Chemotaxis, Endothelium, Humans, Stomach Neoplasms, Up-Regulation, Gene Expression, Gene Expression Regulation, Neoplastic, Immediate-Early Proteins, src-Family Kinases, Phosphatidylinositol 3-Kinases, Receptors, Interleukin-8A, Receptors, Interleukin-8B, Intercellular Signaling Peptides and Proteins, Integrin alpha2beta1, Integrin alpha3beta1, Proto-Oncogene Proteins c-akt, Cysteine-Rich Protein 61
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