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Study · Measured the body's own peptide · 2011

4 results

IGF1Ec expression in MG-63 human osteoblast-like osteosarcoma cells.

Philippou A, Armakolas A, Panteleakou Z, Pissimissis N, Nezos A, Theos A, Kaparelou M, Armakolas N, Pneumaticos SG, Koutsilieris M

Anticancer research1 Dec 2011Cited by 21 (Europe PMC)

PMID22199289 (opens in a new tab)PepBankPUB-22199289

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study4

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

Natural levels measured2

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 01LabEndogenous levelIn vitro (cells)Mechanism

    MG-63 osteosarcoma cells expressed the IGF1Ea and IGF1Ec transcripts only.

    In plain wordsIn cells, human bone cancer cells made only the IGF1Ea and IGF1Ec transcripts, the latter being the body's own MGF form.

    Outcome
    Not applicableIGF1Ec transcript expression in MG-63 cells
    Study

    humann: not reported in source

    MG-63 osteoblast-like osteosarcoma cells
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    MG-63 cells express only the IGF1Ea and IGF1Ec transcripts.
    1 context sentence
    Summary · context
    The aim of this study was to shed light on the expression and role of the IGF1 system in human MG-63 osteoblast-like osteosarcoma cells.

    This result measures the body's own MGF / PEG-MGF. Nobody was given the peptide. It is not evidence about taking it.

  2. 02LabEndogenous levelIn vitro (cells)Mechanism

    Exogenous dihydrotestosterone significantly increased IGF1Ea and IGF1Ec mRNA expression in MG-63 cells.

    In plain wordsIn cells, dihydrotestosterone raised the body's own IGF1Ec mRNA in human bone cancer cells.

    Outcome
    IncreaseIGF1Ec mRNA after dihydrotestosterone
    Study

    humann: not reported in source

    MG-63 osteoblast-like osteosarcoma cells
    Comparator
    Untreated cells
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    Exogenous administration of dihydrotestosterone (DHT) significantly increased the expression of IGF1Ea and IGF1Ec mRNA
    1 context sentence
    Summary · context
    The aim of this study was to shed light on the expression and role of the IGF1 system in human MG-63 osteoblast-like osteosarcoma cells.

    This result measures the body's own MGF / PEG-MGF. Nobody was given the peptide. It is not evidence about taking it.

Studies that did not test the peptide alone2

In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.

  1. 03LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Efficacy outcome

    A synthetic peptide related to the E domain of IGF1Ec stimulated the growth of MG-63 osteosarcoma cells.

    In plain wordsIn cells, a fragment of the IGF1Ec E domain made human bone cancer cells grow more.

    Outcome
    IncreaseMG-63 cell growth with synthetic E peptide
    Study

    humann: not reported in source

    MG-63 osteoblast-like osteosarcoma cells
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    Exogenous administration of IGF1, insulin and the synthetic E peptide stimulated the growth of MG-63 cells, while only E peptide stimulated the growth of IGF1R KO and INSR KO MG-63 cells.
    2 context sentences
    Summary · context
    Using trypan blue exclusion assays, we also examined the mitogenic effects of IGF1 and of a synthetic peptide related to the E domain of IGF1Ec (synthetic E peptide) on MG-63 cells, as well as on MG-63 cells which had been molecularly modified to restrain the expression of type I IGF receptor (IGF1R…
    Summary · context
    The aim of this study was to shed light on the expression and role of the IGF1 system in human MG-63 osteoblast-like osteosarcoma cells.

    In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.

  2. 04LabNot a test of MGF / PEG-MGF aloneIn vitro (cells)Mechanism

    Only the synthetic E peptide, not IGF1 or insulin, stimulated growth of IGF1R KO and INSR KO MG-63 cells.

    In plain wordsIn cells lacking the IGF1 or insulin receptor, only the E peptide fragment still made the cells grow.

    Outcome
    IncreaseGrowth of IGF1R KO and INSR KO MG-63 cells with synthetic E peptide
    Study

    humann: not reported in source

    MG-63 osteoblast-like osteosarcoma cells
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    while only E peptide stimulated the growth of IGF1R KO and INSR KO MG-63 cells.
    2 context sentences
    Summary · context
    Using trypan blue exclusion assays, we also examined the mitogenic effects of IGF1 and of a synthetic peptide related to the E domain of IGF1Ec (synthetic E peptide) on MG-63 cells, as well as on MG-63 cells which had been molecularly modified to restrain the expression of type I IGF receptor (IGF1R…
    Summary · context
    The aim of this study was to shed light on the expression and role of the IGF1 system in human MG-63 osteoblast-like osteosarcoma cells.

    In this study, MGF / PEG-MGF 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 MGF / PEG-MGF.

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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