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
. 1989 Nov;84(5):1418-23.
doi: 10.1172/JCI114315.

Blockade of the type I somatomedin receptor inhibits growth of human breast cancer cells in athymic mice

Affiliations

Blockade of the type I somatomedin receptor inhibits growth of human breast cancer cells in athymic mice

C L Arteaga et al. J Clin Invest. 1989 Nov.

Abstract

Insulin and insulin-like growth factors (IGIs) stimulate the growth of human breast cancer cells in vitro. The type I somatomedin receptor (SR) expressed in these cells may mediate the growth effects of these peptides. We have examined the role of this receptor on human breast cancer growth with a monoclonal antibody (alpha-IR-3) that blocks the receptor binding domain and inhibits IGF-I-induced growth. alpha-IR-3 inhibited clonal growth in vitro and blocked the mitogenic effect of exogenous IGF-I in both MCF-7 and MDA-231 breast cancer cell lines. Antibody-induced blockade of the type I SR also inhibited the estrogen-independent MDA-231 cells growing in vivo in nude mice, but growth of the estrogen-dependent MCF-7 cells was unaffected. IGIs are important growth regulators of MDA-231 breast cancer cells. Blockade of this growth stimulatory pathway may provide a new treatment strategy.

PubMed Disclaimer

References

    1. Proc Natl Acad Sci U S A. 1976 Dec;73(12):4536-40 - PubMed
    1. Mol Endocrinol. 1988 Jun;2(6):543-55 - PubMed
    1. Cancer Res. 1984 Mar;44(3):1002-7 - PubMed
    1. J Biol Chem. 1984 Mar 10;259(5):3090-5 - PubMed
    1. Cancer Res. 1984 May;44(5):2122-8 - PubMed

Publication types

MeSH terms

Substances