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Study · Not a test of the peptide alone · 2009

3 results

Potentiation of growth factor signaling by insulin-like growth factor-binding protein-3 in breast epithelial cells requires sphingosine kinase activity.

Martin JL, Lin MZ, McGowan EM, Baxter RC

The Journal of biological chemistry25 Jul 2009Cited by 71 (Europe PMC)

PMID19633297 (opens in a new tab)PMCIDPMC2757955 (opens in a new tab)DOI10.1074/jbc.m109.007120 (opens in a new tab)PepBankPUB-19633297
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Summary

We have investigated the mechanism underlying potentiation of epidermal growth factor receptor (EGFR) and type 1 insulin-like growth factor receptor (IGFR1) signaling by IGF-binding protein-3 (IGFBP-3) in MCF-10A breast epithelial cells, focusing on a possible involvement of the sphingosine kinase (SphK) system. IGFBP-3 potentiated EGF-stimulated EGF receptor activation and DNA synthesis, and this was blocked by inhibitors of SphK activity or small interference RNA-mediated silencing of SphK1, but not SphK2, expression. Similarly, IGFR1 phosphorylation and DNA synthesis stimulated by LR3-IGF-I (an IGF-I analog not bound by IGFBP-3), were enhanced by IGFBP-3, and this was blocked by SphK1 silencing. SphK1 expression and activity were stimulated by IGFBP-3 approximately 2-fold over 24 h. Silencing of sphingosine 1-phosphate receptor 1 (S1P1) or S1P3, but not S1P2, abolished the effect of IGFBP-3 on EGF-stimulated EGFR activation. The effects of IGFBP-3 could be reproduced with exogenous S1P or medium conditioned by cells treated with IGFBP-3, and this was also blocked by inhibition of S1P1 and S1P3. These data indicate that potentiation of growth factor signaling by IGFBP-3 in MCF-10A cells requires SphK1 activity and S1P1/S1P3, suggesting that S1P, the product of SphK activity and ligand for S1P1 and S1P3, is the "missing link" mediating IGF and EGFR transactivation and cell growth stimulation by IGFBP-3.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study3

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone3

In this study, IGF-1 LR3 was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking IGF-1 LR3.

  1. 01LabNot a test of IGF-1 LR3 aloneIn vitro (cells)Mechanism

    In MCF-10A cells, IGFBP-3 enhanced IGFR1 phosphorylation stimulated by LR3-IGF-I.

    In plain wordsIn breast cells grown in the lab, IGFBP-3 boosted receptor activation caused by LR3-IGF-I.

    Peptide
    IGF-1 LR3
    Outcome
    IncreaseIGFBP-3 enhancement of LR3-IGF-I-stimulated IGFR1 phosphorylation
    Study

    n: not reported in source

    MCF-10A breast epithelial cells
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    Similarly, IGFR1 phosphorylation and DNA synthesis stimulated by LR3-IGF-I (an IGF-I analog not bound by IGFBP-3), were enhanced by IGFBP-3, and this was blocked by SphK1 silencing.
    1 context sentence
    Summary · context
    We have investigated the mechanism underlying potentiation of epidermal growth factor receptor (EGFR) and type 1 insulin-like growth factor receptor (IGFR1) signaling by IGF-binding protein-3 (IGFBP-3) in MCF-10A breast epithelial cells, focusing on a possible involvement of the sphingosine kinase (SphK) system.

    In this study, IGF-1 LR3 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking IGF-1 LR3.

  2. 02LabNot a test of IGF-1 LR3 aloneIn vitro (cells)Mechanism

    In MCF-10A cells, IGFBP-3 enhanced DNA synthesis stimulated by LR3-IGF-I.

    In plain wordsIn breast cells grown in the lab, IGFBP-3 boosted DNA synthesis stimulated by LR3-IGF-I.

    Peptide
    IGF-1 LR3
    Outcome
    IncreaseIGFBP-3 enhancement of LR3-IGF-I-stimulated DNA synthesis
    Study

    n: not reported in source

    MCF-10A breast epithelial cells
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    Similarly, IGFR1 phosphorylation and DNA synthesis stimulated by LR3-IGF-I (an IGF-I analog not bound by IGFBP-3), were enhanced by IGFBP-3, and this was blocked by SphK1 silencing.
    1 context sentence
    Summary · context
    We have investigated the mechanism underlying potentiation of epidermal growth factor receptor (EGFR) and type 1 insulin-like growth factor receptor (IGFR1) signaling by IGF-binding protein-3 (IGFBP-3) in MCF-10A breast epithelial cells, focusing on a possible involvement of the sphingosine kinase (SphK) system.

    In this study, IGF-1 LR3 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking IGF-1 LR3.

  3. 03LabNot a test of IGF-1 LR3 aloneIn vitro (cells)Mechanism

    In MCF-10A cells, SphK1 silencing blocked the IGFBP-3 enhancement of LR3-IGF-I-stimulated IGFR1 phosphorylation and DNA synthesis.

    In plain wordsIn breast cells grown in the lab, silencing SphK1 blocked the boost that IGFBP-3 gave to LR3-IGF-I signaling.

    Peptide
    IGF-1 LR3
    Outcome
    DecreaseSphK1 silencing block of IGFBP-3 enhancement of LR3-IGF-I signaling
    Study

    n: not reported in source

    MCF-10A breast epithelial cells
    Outcome group
    Receptor activity and mechanism · Cancer

    Source sentences

    Summary
    Similarly, IGFR1 phosphorylation and DNA synthesis stimulated by LR3-IGF-I (an IGF-I analog not bound by IGFBP-3), were enhanced by IGFBP-3, and this was blocked by SphK1 silencing.
    1 context sentence
    Summary · context
    We have investigated the mechanism underlying potentiation of epidermal growth factor receptor (EGFR) and type 1 insulin-like growth factor receptor (IGFR1) signaling by IGF-binding protein-3 (IGFBP-3) in MCF-10A breast epithelial cells, focusing on a possible involvement of the sphingosine kinase (SphK) system.

    In this study, IGF-1 LR3 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking IGF-1 LR3.

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    13 Oct 2026, 21:44 UTC

    Study results updated

  2. Version 1

    13 Oct 2026, 16:31 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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