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Study · Measured the body's own peptide · 2007

6 results

Thymosin beta4 triggers an epithelial-mesenchymal transition in colorectal carcinoma by upregulating integrin-linked kinase.

Huang HC, Hu CH, Tang MC, Wang WS, Chen PM, Su Y

Oncogene30 Oct 2006Cited by 76 (Europe PMC)

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 study6

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

Natural levels measured1

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. 01HumanEndogenous levelObservational studyMechanism

    In colorectal carcinoma patients, immunohistochemistry showed a strong correlation between expression levels of the body's own Tbeta4, ILK and E-cadherin.

    In plain wordsIn people with colorectal cancer, natural thymosin beta4 levels in tumors were strongly linked to ILK and E-cadherin levels.

    Outcome
    Not applicableCorrelation of Tbeta4, ILK and E-cadherin expression in CRC patients
    Study

    n: not reported in source

    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    In the meantime, a strong correlation between the expression levels of Tbeta4, ILK and E-cadherin in CRC patients was also revealed by immunohistochemical analysis.

    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 alone5

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. 02LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In SW480 colon cancer cells overexpressing thymosin beta4, cells showed a scattering, fibroblastic morphology with reduced intercellular contacts.

    In plain wordsIn cells, colon cancer cells making extra thymosin beta4 looked scattered and fibroblast-like with fewer cell contacts.

    Outcome
    Not applicableCell morphology and EMT in Tbeta4-overexpressing SW480 cells
    Study

    humann: not reported in source

    SW480 colon cancer cells
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    a scattering and fibroblastic morphology with reduced intercellular contacts was found in the SW480 colon cancer cells overexpressing the gene encoding thymosin beta4 (Tbeta4)

    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).

  2. 03LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    SW480 colon cancer cells overexpressing thymosin beta4 lost E-cadherin, an EMT marker.

    In plain wordsIn cells, colon cancer cells making extra thymosin beta4 lost E-cadherin, a marker of epithelial-mesenchymal transition.

    Outcome
    DecreaseE-cadherin level in Tbeta4-overexpressing SW480 cells
    Study

    humann: not reported in source

    SW480 colon cancer cells
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    In the present study, a scattering and fibroblastic morphology with reduced intercellular contacts was found in the SW480 colon cancer cells overexpressing the gene encoding thymosin beta4 (Tbeta4), which was accompanied by a loss of E-cadherin as well as a cytosolic accumulation of beta-catenin, tw…

    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).

  3. 04LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    SW480 colon cancer cells overexpressing thymosin beta4 showed cytosolic accumulation of beta-catenin, an EMT marker.

    In plain wordsIn cells, colon cancer cells making extra thymosin beta4 built up beta-catenin in the cell fluid.

    Outcome
    IncreaseCytosolic beta-catenin in Tbeta4-overexpressing SW480 cells
    Study

    humann: not reported in source

    SW480 colon cancer cells
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    In the present study, a scattering and fibroblastic morphology with reduced intercellular contacts was found in the SW480 colon cancer cells overexpressing the gene encoding thymosin beta4 (Tbeta4), which was accompanied by a loss of E-cadherin as well as a cytosolic accumulation of beta-catenin, tw…

    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).

  4. 05LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In Tbeta4-overexpressing SW480 cells, beta-catenin accumulation resulted from glycogen synthase kinase-3beta inactivation mediated by integrin-linked kinase and/or Akt.

    In plain wordsIn cells, extra thymosin beta4 led to beta-catenin build-up through a switched-off enzyme, GSK-3beta, driven by ILK and Akt.

    Outcome
    Not applicableGSK-3beta inactivation via ILK and Akt
    Study

    humann: not reported in source

    SW480 colon cancer cells
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    the accumulation of beta-catenin was a result of glycogen synthase kinase-3beta inactivation mediated by integrin-linked kinase (ILK) and/or its downstream effector, Akt.

    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).

  5. 06LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism

    In Tbeta4-overexpressing SW480 cells, integrin-linked kinase was upregulated, apparently through stabilization by complexing with PINCH.

    In plain wordsIn cells, extra thymosin beta4 raised integrin-linked kinase levels, apparently by making the kinase more stable.

    Outcome
    IncreaseILK upregulation and stabilization with PINCH
    Study

    humann: not reported in source

    SW480 colon cancer cells
    Outcome group
    Tumor growth · Cancer

    Source sentences

    Summary
    Intriguingly, ILK upregulation in Tbeta4-overexpressing SW480 cells seemed to be attributed mainly to a stabilization of this kinase by complexing with particularly interesting new Cys-His protein (PINCH) more efficiently.

    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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