Induction of anchorage-independent growth by amphiregulin
Induction of anchorage-independent growth by amphiregulin
We have previously shown that the epidermal growth factor receptor (EGFR) ligand, amphiregulin (AR) exhibits low potency as a result of its C-terminal truncation. This led us to investigate whether its inability to promote anchorage-independent growth (AIG) of normal cells arose because of its compromised interaction with EGFR. Wild type AR., was tested in AIG and mitogenesis assays using NRK-49F or NR6/HER fibroblasts. In contrast to NR6/HER cells, the response of NRK-49F fibroblasts to AR was much lower than expected. As the effect of AR was heparin-insensitive, contributions from heparan sulphate proteoglycan interactions could not explain the differing sensitivities of the cells. Comparison of the effects of AR on two additional cell lines indicated that low EGFR number correlated with AR insensitivity: this suggested that the low potency of AR precluded activation of sufficient receptors to elicit a response.Consistent with this proposal, a modified form of AR (AR1-90(leu86)) with enhanced potency was able to induce AIG of NRK-49F fibroblasts. Thus, the ability of AR to promote AIG is determined both by ligand potency and the EGFR complement of cells.
Amphiregulin, EGF, EGF receptor, Epidermal growth factor, Heparin binding growth factors
193-203
Adam, Rosalyn M.
4a44ecf1-de31-45ff-bf4e-70764495aab9
Chamberlin, Stephen G.
ecb947dd-c59e-4c1d-b1f5-60aff91fbeb0
Davies, Donna E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
1 June 1996
Adam, Rosalyn M.
4a44ecf1-de31-45ff-bf4e-70764495aab9
Chamberlin, Stephen G.
ecb947dd-c59e-4c1d-b1f5-60aff91fbeb0
Davies, Donna E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Adam, Rosalyn M., Chamberlin, Stephen G. and Davies, Donna E.
(1996)
Induction of anchorage-independent growth by amphiregulin.
Growth Factors, 13 (3-4), .
(doi:10.3109/08977199609003221).
Abstract
We have previously shown that the epidermal growth factor receptor (EGFR) ligand, amphiregulin (AR) exhibits low potency as a result of its C-terminal truncation. This led us to investigate whether its inability to promote anchorage-independent growth (AIG) of normal cells arose because of its compromised interaction with EGFR. Wild type AR., was tested in AIG and mitogenesis assays using NRK-49F or NR6/HER fibroblasts. In contrast to NR6/HER cells, the response of NRK-49F fibroblasts to AR was much lower than expected. As the effect of AR was heparin-insensitive, contributions from heparan sulphate proteoglycan interactions could not explain the differing sensitivities of the cells. Comparison of the effects of AR on two additional cell lines indicated that low EGFR number correlated with AR insensitivity: this suggested that the low potency of AR precluded activation of sufficient receptors to elicit a response.Consistent with this proposal, a modified form of AR (AR1-90(leu86)) with enhanced potency was able to induce AIG of NRK-49F fibroblasts. Thus, the ability of AR to promote AIG is determined both by ligand potency and the EGFR complement of cells.
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Published date: 1 June 1996
Keywords:
Amphiregulin, EGF, EGF receptor, Epidermal growth factor, Heparin binding growth factors
Identifiers
Local EPrints ID: 470304
URI: http://eprints.soton.ac.uk/id/eprint/470304
ISSN: 0897-7194
PURE UUID: bace3894-91be-4b70-8674-7314ac1ac671
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Date deposited: 06 Oct 2022 16:30
Last modified: 17 Mar 2024 02:33
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Author:
Rosalyn M. Adam
Author:
Stephen G. Chamberlin
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