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
. 2020 Jun 23;21(12):4449.
doi: 10.3390/ijms21124449.

Cytokines and Chemokines as Mediators of Prostate Cancer Metastasis

Affiliations
Review

Cytokines and Chemokines as Mediators of Prostate Cancer Metastasis

Timothy O Adekoya et al. Int J Mol Sci. .

Abstract

The consequences of prostate cancer metastasis remain severe, with huge impact on the mortality and overall quality of life of affected patients. Despite the convoluted interplay and cross talk between various cell types and secreted factors in the metastatic process, cytokine and chemokines, along with their receptors and signaling axis, constitute important factors that help drive the sequence of events that lead to metastasis of prostate cancer. These proteins are involved in extracellular matrix remodeling, epithelial-mesenchymal-transition, angiogenesis, tumor invasion, premetastatic niche creation, extravasation, re-establishment of tumor cells in secondary organs as well as the remodeling of the metastatic tumor microenvironment. This review presents an overview of the main cytokines/chemokines, including IL-6, CXCL12, TGFβ, CXCL8, VEGF, RANKL, CCL2, CX3CL1, IL-1, IL-7, CXCL1, and CXCL16, that exert modulatory roles in prostate cancer metastasis. We also provide extensive description of their aberrant expression patterns in both advanced disease states and metastatic sites, as well as their functional involvement in the various stages of the prostate cancer metastatic process.

Keywords: chemokines; cytokines; metastasis; prostate cancer.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Schematic showing the process of prostate cancer cell metastasis and the involvement of various cytokines and chemokines along the sequence of event.

Similar articles

Cited by

References

    1. Shen M.M., Abate-Shen C. Molecular genetics of prostate cancer: New prospects for old challenges. Genes Dev. 2010;24:1967–2000. doi: 10.1101/gad.1965810. - DOI - PMC - PubMed
    1. Feldman B.J., Feldman D. The development of androgen-independent prostate cancer. Nat. Rev. Cancer. 2001;1:34–45. doi: 10.1038/35094009. - DOI - PubMed
    1. Litwin M.S., Tan H.J. The Diagnosis and Treatment of Prostate Cancer: A Review. JAMA. 2017;317:2532–2542. doi: 10.1001/jama.2017.7248. - DOI - PubMed
    1. Karantanos T., Corn P.G., Thompson T.C. Prostate cancer progression after androgen deprivation therapy: Mechanisms of castrate resistance and novel therapeutic approaches. Oncogene. 2013;32:5501–5511. doi: 10.1038/onc.2013.206. - DOI - PMC - PubMed
    1. Wang Q., Li W., Zhang Y., Yuan X., Xu K., Yu J., Chen Z., Beroukhim R., Wang H., Lupien M., et al. Androgen receptor regulates a distinct transcription program in androgen-independent prostate cancer. Cell. 2009;138:245–256. doi: 10.1016/j.cell.2009.04.056. - DOI - PMC - PubMed