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Study · Measured the body's own peptide · 2012

4 results

Regulation of glycogen synthase kinase-3 by thymosin beta-4 is associated with gastric cancer cell migration.

Ryu YK, Lee YS, Lee GH, Song KS, Kim YS, Moon EY

International journal of cancer28 Mar 2012Cited by 39 (Europe PMC)

PMID22328534 (opens in a new tab)DOI10.1002/ijc.27490 (opens in a new tab)PepBankPUB-22328534
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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 measured3

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 levelEx vivo tissueMechanism

    Various expression levels of Tβ4 were observed in human gastric tumor tissues.

    In plain wordsIn human stomach tumour samples, the body's own Tβ4 level varied between samples.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    Not applicableTβ4 expression level in gastric tumor tissue
    Study

    humann: not reported in source

    gastric tumor tissue
    Outcome group
    Gene expression · Cancer

    Source sentences

    Summary
    Various expression level of Tβ4 was observed in human gastric tumor tissues.
    1 context sentence
    Summary · context
    Here, we investigated whether GSK-3 activity is regulated by Tβ4 and it is associated with Tβ4-mediated migration in gastric cancer cells.

    This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.

  2. 02LabEndogenous levelIn vitro (cells)Mechanism

    Cell migration was higher in SNU668 cells, which express more Tβ4, than in SNU638 cells, which express less.

    In plain wordsIn lab-grown stomach cancer cells, cells with more of their own Tβ4 moved more than cells with less.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    IncreaseCell migration by Tβ4 expression level
    Study

    humann: not reported in source

    SNU638 and SNU668 gastric cancer cells
    Comparator
    SNU638 (lower Tβ4)
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    Cell migration was higher in SNU668 with a higher expression level of Tβ4 than that in SNU638 with a lower Tβ4.
    1 context sentence
    Summary · context
    Here, we investigated whether GSK-3 activity is regulated by Tβ4 and it is associated with Tβ4-mediated migration in gastric cancer cells.

    This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.

  3. 03LabEndogenous levelIn vitro (cells)Mechanism

    In SNU638 gastric cancer cells, which express less Tβ4, phosphorylated GSK-3α, β-catenin, E-cadherin and the E-cadherin:β-catenin complex were relatively higher and phosphorylated GSK-3β was lower than in SNU668 cells.

    In plain wordsIn lab-grown stomach cancer cells, cells with less of their own Tβ4 had higher levels of some signalling proteins and a lower level of one.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    MixedSignalling protein levels in gastric cancer cells with lower versus higher Tβ4
    Study

    humann: not reported in source

    SNU638 and SNU668 gastric cancer cells
    Comparator
    SNU668 (higher Tβ4)
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    Although the level of phosphorylated(p)-GSK-3α (inactive), β-catenin, E-cadherin and E-cadherin:β-catenin complex was relatively higher, p-GSK-3β (inactive) was lower in SNU638 compared to those in SNU668 cells.

    This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.

Studies that did not test the peptide alone1

In this study, Thymosin beta-4 (human) 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 Thymosin beta-4 (human).

  1. 04LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In gastric cancer cells, Tβ4-siRNA and SDKP tetrapeptide treatment reversed the expression level of GSK-3α/β, β-catenin and E-cadherin.

    In plain wordsIn lab-grown stomach cancer cells, silencing Tβ4 or adding its SDKP piece reversed levels of three signalling proteins.

    Peptide
    Thymosin beta-4 (human)
    Outcome
    MixedGSK-3α/β, β-catenin and E-cadherin expression after Tβ4 knockdown
    Study

    humann: not reported in source

    SNU668 and SNU638 gastric cancer cells
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    Expression level of GSK-3α/β, β-catenin and E-cadherin in SNU668 and SNU638 was reversed by Tβ4-siRNA and by the treatment with acetylated-serine-aspartic acid-lysine-proline (SDKP) tetrapeptide of Tβ4, respectively.
    1 context sentence
    Summary · context
    Here, we investigated whether GSK-3 activity is regulated by Tβ4 and it is associated with Tβ4-mediated migration in gastric cancer cells.

    In this study, Thymosin beta-4 (human) 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 Thymosin beta-4 (human).

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, 01:52 UTC

    Study results updated

  2. Version 1

    12 Oct 2026, 18:17 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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