Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2013 May 21;19(19):2847-63.
doi: 10.3748/wjg.v19.i19.2847.

Chemokines, chemokine receptors and the gastrointestinal system

Affiliations
Review

Chemokines, chemokine receptors and the gastrointestinal system

Hiroshi Miyazaki et al. World J Gastroenterol. .

Abstract

The biological properties of tumor cells are known to be regulated by a multitude of cytokines and growth factors, which include epidermal growth factor receptor agonists and members of the transforming growth factor β family. Furthermore, the recent explosion of research in the field of chemokine function as mediators of tumor progression has led to the possibility that these small, immunomodulatory proteins also play key roles in carcinogenesis and may, therefore, be potential targets for novel therapeutic approaches. In this review, we will summarize recently reported findings in chemokine biology with a focus on the gastrointestinal tract.

Keywords: Cancer; Chemokine; Digestive system; Receptor; Signal transduction; Targeted therapeutics; Tumor progression.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Chemokine-induced signal transduction pathways. Schematic representation of signaling pathways activated by binding of chemokine ligands to their seven transmembrane G-protein coupled receptors. MMPs: Matrix metalloproteinases; TFs: Transcription factors; RTK: Receptor tyrosine kinase; ERK: Extracellular signal-regulated kinase; MEK: Mitogen-activated protein/extracellular signal-regulated kinase kinase; PI-3K: Phosphatidyl inositide-3-OH kinase; MKK: Mitogen-activated protein kinase kinase; JNK: c-Jun N-terminal kinase; AKT: Protein kinase B.

Similar articles

Cited by

References

    1. Egger G, Liang G, Aparicio A, Jones PA. Epigenetics in human disease and prospects for epigenetic therapy. Nature. 2004;429:457–463. - PubMed
    1. Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 2011;144:646–674. - PubMed
    1. Christofori G. New signals from the invasive front. Nature. 2006;441:444–450. - PubMed
    1. Alexiou C, Khan OA, Black E, Field ML, Onyeaka P, Beggs L, Duffy JP, Beggs DF. Survival after esophageal resection for carcinoma: the importance of the histologic cell type. Ann Thorac Surg. 2006;82:1073–1077. - PubMed
    1. Tait CR, Waterworth A, Loncaster J, Horgan K, Dodwell D. The oligometastatic state in breast cancer: hypothesis or reality. Breast. 2005;14:87–93. - PubMed

MeSH terms