Suramin inhibition of growth factor receptor binding and mitogenicity in AKR‐2B cells

Authors:
  • RCRobert J. Coffey
    Robert J. Coffey
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Abstract
Suramin, a polyanionic compound, has previously been shown to dissociate platelet‐derived growth factor (PDGF) from its receptor. In the present study suramin was found to inhibit the growth of sparse cultures of AKR‐2B cells in fetal bovine serum (FBS)‐supplemented medium in a dose‐dependent, reversible fashion. Suramin also inhibited the ability of FBS, transforming growth factor β (TGFβ), heparin‐binding growth factor type‐2 (HBGF‐2), and epidermal growth factor (EGF) to stimulate DNA synthesis in density‐arrested cultures of AKR‐2B cells. The inhibition of growth factor‐stimulated mitogenicity was directly correlated to the dose of suramin required to inhibit the binding of 125I‐labeled TGFβ, HBGF‐2, and EGF to their cell surface receptors. Suramin affected TGFβ and HBGF‐2‐related events at a 10–15‐fold lower dose than that required for EGF‐related events. It was also noted that suramin inhibited TGFβ‐stimulated soft agar colony formation of AKR‐2B (clone 84A) cells as well as the spontaneous colony formation of AKR‐MCA cells, a chemically transformed derivative of AKR‐2B cells. This demonstrates that suramin's spectrum of action for growth factors and their receptors should be extended to include TGFβ, HBGF‐2, and EGF as well as PDGF. The data further suggest that the spontaneous growth of AKR‐MCA cells in soft agar is dependent on growth factor binding to cell surface receptors.

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