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Science 29 June 1990:
Vol. 248. no. 4963, pp. 1656 - 1660
DOI: 10.1126/science.2163544
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Articles

Science, Vol 248, Issue 4963, 1656-1660
Copyright © 1990 by American Association for the Advancement of Science

articles

Mediation of wound-related Rous sarcoma virus tumorigenesis by TGF-beta

MH Sieweke, NL Thompson, MB Sporn, and MJ Bissell

Cell and Molecular Biology Division, Lawrence Berkeley Laboratory, University of California, Berkeley 94720.

In Rous sarcoma virus (RSV)-infected chickens, wounding leads to tumor formation with nearly 100% frequency in tissues that would otherwise remain tumor-free. Identifying molecular mediators of this phenomenon should yield important clues to the mechanisms involved in RSV tumorigenesis. Immunohistochemical staining showed that TGF-beta is present locally shortly after wounding, but not unwounded controls. In addition, subcutaneous administration of recombinant transforming growth factor-beta 1 (TGF-beta 1) could substitute completely for wounding in tumor induction. A treatment protocol of four doses of 800 nanograms of TGF-beta resulted in v-src-expressing tumors with 100% frequency; four doses of only 10 nanograms still led to tumor formation in 80% of the animals. This effect was specific, as other growth factors with suggested roles in wound healing did not elicit the same response. Epidermal growth factor (EGF) or TGF-alpha had no effect, and platelet-derived growth factor (PDGF) or insulin-like growth factor-1 (IGF-1) yielded only occasional tumors after longer latency. TGF-beta release during the wound-healing response may thus be a critical event that creates a conducive environment for RSV tumorigenesis and may act as a cofactor for transformation in this system.


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