The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index.
Suramin inhibition of growth factor receptor binding and mitogenicity in AKR‐2B cells
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 125 I‐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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Cites
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Epidermal Growth Factor and a New Derivative
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Growth Inhibitor from BSC-1 Cells Closely Related to Platelet Type β Transforming Growth Factor
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Self-citationSuramin Protection of T Cells in Vitro Against Infectivity and Cytopathic Effect of HTLV-III
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Cited by
Mignatti, P., Morimoto, T., & Rifkin, D. B. (1992) · Journal of Cellular Physiology · doi:10.1002/jcp.1041510113 · Cited by 451
Use of suramin in treatment of prostatic carcinoma refractory to conventional hormonal manipulation
LaRocca, R. V., Cooper, M. R., Uhrich, M., Danesi, R., Walther, M. M., Linehan, W. M., & Myers, C. E. (1991) · Urologic Clinics of North America · doi:10.1016/s0094-0143(21)01399-9 · Cited by 57
Suramin in adrenocortical cancer: limited efficacy and serious toxicity
Arlt, W., Reincke, M., Siekmann, L., WInkelmann, W., & Allolio, B. (1994) · Clinical Endocrinology · doi:10.1111/j.1365-2265.1994.tb02549.x · Cited by 36
Metadata
- Authors
- Coffey, R. J., Leof, E. B., Shipley, G. D., & Moses, H. L.
- Venue
- Journal of Cellular Physiology
- Publisher
- Wiley
- Published
- 1987-07
- Volume
- 132
- Issue
- 1
- Pages
- 143-148
- ISSN
- 0021-9541 (ISSN-L)
- 1097-4652
- OpenAlex
- W1967642037
- Cited by
- 379
- References
- 23
- FWCI
- 6.21
- Type
- journal article
- Language
- en
- Open access
- closed
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- Coffey, R. J., Leof, E. B., Shipley, G. D., & Moses, H. L. (1987). Suramin inhibition of growth factor receptor binding and mitogenicity in AKR‐2B cells. Journal of Cellular Physiology. https://doi.org/10.1002/jcp.1041320120
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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