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Breast Cancer Res Treat. 1992;22(1):39-45. doi: 10.1007/BF01833332.

IGF-I and IGF-II expression in human breast cancer xenografts: relationship to hormone independence.

Breast cancer research and treatment

N Brünner, C Moser, R Clarke, K Cullen

Affiliations

  1. Finsen Laboratory, Rigshospitalet, Copenhagen, Denmark.

PMID: 1421423 DOI: 10.1007/BF01833332

Abstract

Although the growth of some estrogen receptor (ER) positive breast cancers can initially be hormonally manipulated, all will eventually escape hormonal control. It is possible that the expression of polypeptide growth factors is initially under the control of steroid hormones, while the hormone unresponsive state is characterized by constitutive expression of growth factors. We studied the relationship between hormone responsiveness and IGF expression in xenograft models. The ER+ T61 xenograft was established from a primary breast cancer and has been continually passaged in athymic mice. ER+ MCF-7 cells and ER-MDA-MB-231 cells were grown in tissue culture and then inoculated into athymic mice. ER+ xenograft growth was regulated by estrogen, but with opposite results--T61 xenografts are inhibited by estrogen, while MCF-7 xenografts require estrogen for tumor formation. All xenografts expressed type I and II IGF receptors. Although T61 xenografts also express an alternatively spliced IGF-I mRNA, its expression was not regulated by estrogen. Both xenografts expressed IGF-II in a hormonally regulated manner--T61 levels were depressed by estrogen, while MCF-7 levels were increased. Thus, in these model systems, xenograft regulation of tumor growth is accompanied by parallel changes in IGF-II expression. In the estrogen independent MDA-MB-231 cells, IGF-II was constitutively expressed. These data show that IGF-II expression correlates with estrogen treatment, suggesting that autocrine expression of IGF-II may mediate estrogen-regulated cell growth.

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References

  1. Biochem Biophys Res Commun. 1988 Apr 15;152(1):398-405 - PubMed
  2. J Cell Biochem. 1990 Jul;43(3):199-211 - PubMed
  3. Proc Natl Acad Sci U S A. 1989 May;86(10):3649-53 - PubMed
  4. Breast Cancer Res Treat. 1987 Dec;10(3):229-42 - PubMed
  5. Cancer Res. 1988 Dec 1;48(23):6691-6 - PubMed
  6. Cancer Cells. 1989 Nov;1(3):81-6 - PubMed
  7. Cancer Res. 1993 Jan 15;53(2):283-90 - PubMed
  8. J Clin Invest. 1989 Nov;84(5):1418-23 - PubMed
  9. Mol Endocrinol. 1989 Mar;3(3):509-17 - PubMed
  10. Endocr Rev. 1987 Feb;8(1):29-43 - PubMed
  11. Cancer Res. 1990 Jan 1;50(1):48-53 - PubMed
  12. Cell. 1987 Feb 13;48(3):417-28 - PubMed
  13. Proc Natl Acad Sci U S A. 1984 Oct;81(20):6344-8 - PubMed
  14. Mol Endocrinol. 1988 Jun;2(6):543-55 - PubMed
  15. Eur J Cancer. 1993;29A(4):562-9 - PubMed
  16. Cancer Res. 1984 Dec;44(12 Pt 1):5486-90 - PubMed
  17. Mol Endocrinol. 1990 Dec;4(12):1914-20 - PubMed
  18. Cancer Res. 1988 Nov 15;48(22):6429-33 - PubMed
  19. Am J Pathol. 1989 Dec;135(6):961-6 - PubMed
  20. Biochem Biophys Res Commun. 1987 Nov 30;149(1):276-81 - PubMed
  21. J Steroid Biochem. 1986 Sep;25(3):429-32 - PubMed

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