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. 2012 Dec 1;2(12):a006676.
doi: 10.1101/cshperspect.a006676.

The role of the tumor microenvironment in regulating angiogenesis

Randolph S Watnick  1
Affiliations

The role of the tumor microenvironment in regulating angiogenesis

Randolph S Watnick. Cold Spring Harb Perspect Med. .

Abstract

The tumor-associated stroma has been shown to play a significant role in cancer formation. Paracrine signaling interactions between epithelial tumor cells and stromal cells are a key component in the transformation and proliferation of tumors in several organs. Whereas the intracellular signaling pathways regulating the expression of several pro- and antiangiogenic proteins have been well characterized in human cancer cells, the intercellular signaling that takes place between tumor cells and the surrounding tumor-associated stroma has not been as extensively studied with regard to the regulation of angiogenesis. In this chapter we define the key players in the regulation of angiogenesis and examine how their expression is regulated in the tumor-associated stroma. The resulting analysis is often seemingly paradoxical, underscoring the complexity of intercellular signaling within tumors and the need to better understand the environmental context underlying these signaling mechanisms.

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Figures

Figure 1.
Figure 1.
Schematic of tumor microenvironment.
Figure 2.
Figure 2.
Tumor–stromal paracrine signaling. Tumors secrete factors into the microenvironment that act on the stromal cells to either promote or inhibit the growth of new blood vessels (angiogenesis).
See this image and copyright information in PMC

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References

    1. Abraham JA, Mergia A, Whang JL, Tumolo A, Friedman J, Hjerrild KA, Gospodarowicz D, Fiddes JC 1986. Nucleotide sequence of a bovine clone encoding the angiogenic protein, basic fibroblast growth factor. Science 233: 545–548 - PubMed
    1. Ai S, Cheng XW, Inoue A, Nakamura K, Okumura K, Iguchi A, Murohara T, Kuzuya M 2007. Angiogenic activity of bFGF and VEGF suppressed by proteolytic cleavage by neutrophil elastase. Biochem Biophys Res Commun 364: 395–401 - PubMed
    1. Akiyama H, Tanaka T, Maeno T, Kanai H, Kimura Y, Kishi S, Kurabayashi M 2002. Induction of VEGF gene expression by retinoic acid through Sp1–binding sites in retinoblastoma Y79 cells. Invest Ophthalmol Vis Sci 43: 1367–1374 - PubMed
    1. Aljada A, O'Connor L, Fu YY, Mousa SA 2008. PPAR γ ligands, rosiglitazone and pioglitazone, inhibit bFGF- and VEGF-mediated angiogenesis. Angiogenesis 11: 361–367 - PubMed
    1. Baird A, Durkin T 1986. Inhibition of endothelial cell proliferation by type beta-transforming growth factor: Interactions with acidic and basic fibroblast growth factors. Biochem Biophys Res Commun 138: 476–482 - PubMed

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