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
. 2009 May 1;69(9):3727-30.
doi: 10.1158/0008-5472.CAN-08-4289. Epub 2009 Apr 21.

Catecholamines regulate tumor angiogenesis

Affiliations
Review

Catecholamines regulate tumor angiogenesis

Debanjan Chakroborty et al. Cancer Res. .

Abstract

Among the regulators of angiogenesis, catecholamine neurotransmitters are of recent interest because of their opposite roles in the regulation of tumor neovascularization. Norepinephrine and epinephrine by acting through specific adrenoceptors increase the synthesis of proangiogenic factors, and thereby, promote tumor growth. In contrast, dopamine acting via its specific D(2) receptors inhibits tumor growth by suppressing the actions of vascular permeability factor/vascular endothelial growth factor-A on both tumor endothelial and bone marrow-derived endothelial progenitor cells. These reports identify novel endogenous regulators of tumor angiogenesis and also indicate a new and an inexpensive class of antiangiogenic drugs for the treatment of cancer.

PubMed Disclaimer

Conflict of interest statement

Disclosure of Potential Conflicts of Interest

No potential conflicts of interest were disclosed.

Figures

Figure 1.
Figure 1.
Schematic diagram of norepinephrine- and dopamine-mediated signaling pathways in tumor cells, endothelial cells, and endothelial progenitor cells that regulate tumor angiogenesis. A, norepinephrine acting through β adrenoceptors in ovarian carcinoma cells induces synthesis and release of proangiogenic molecules, IL-6, and VEGF by these cells. B, dopamine acting through D2 receptors in tumor endothelial cells inhibits proliferation of these cells by inhibiting phosphorylation of VEGFR-2, MAPK, and FAK. C, dopamine acting through D2 receptors decreases ERK1/ERK2-mediated MMP-9 release by endothelial progenitor cells and thereby inhibits their mobilization from the bone marrow and thus prevents their participation in tumor neovascularization. βAR, βadrenergic receptor; EC, endothelial cell; EPC, endothelial progenitor cell; BM, bone marrow; VEGFR-2, vascular endothelial growth factor receptor 2; MAPK, MAP kinase; FAK, focal adhesion kinase; MMP-9, matrix metalloproteinase-9.

Similar articles

Cited by

References

    1. Dvorak HF. Angiogenesis: update 2005. J Thromb Haemost 2005;3:1835–42. doi:10.1111/j.1538-7836.2005.01361.x. - DOI - PubMed
    1. Asahara T, Masuda H, Takahashi T, et al. Bone marrow origin of endothelial progenitor cells responsible for postnatal vasculogenesis in physiological and pathological neovascularization. Circ Res 1999;85:221–8. - PubMed
    1. Heissig B, Hattori K, Dias S, et al. Recruitment of stem and progenitor cells from the bone marrow niche requires MMP-9 mediated release of kit-ligand. Cell 2002; 109: 625–37. doi:10.1016/S0092-8674(02)00754-7. - DOI - PMC - PubMed
    1. Ferrara N, Kerbel RS. Angiogenesis as a therapeutic target. Nature 2005;438:967–74. doi:10.1038/nature04483. - DOI - PubMed
    1. Ellis LM, Hicklin DJ. VEGF-targeted therapy: mechanisms of anti-tumour activity. Nat Rev Cancer 2008; 8:579–91. doi:10.1038/nrc2403. - DOI - PubMed

Publication types

MeSH terms