In vivo CRISPR-Cas9 knockout screening using quantitative PCR identifies thymosin beta-4 X-linked that promotes diffuse-type gastric cancer metastasis.

An HW, Kim SY, Kwon JW, Seok SH, Woo SH, Kim DY, Park JW

Molecular carcinogenesis3 Jun 2021Cited by 18 (Europe PMC)

PMID34081824DOI10.1002/mc.23326PepBankPUB-34081824

Publisher page PubMedAsk about this study

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 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.

01AnimalEndogenous levelAnimal study (in vivo)Other
In situ hybridization showed that Tmsb4x is more highly expressed in E-cadherin-negative mouse diffuse-type gastric cancer models than in intestinal-type gastric and intestinal cancer models.
In plain wordsIn mice, the body's own Tmsb4x gene was more active in diffuse-type stomach cancer models than in intestinal-type models.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseTmsb4x expression in E-cadherin-negative diffuse-type models
Study
mousen: not reported in source
mouse diffuse-type gastric cancer models lacking Smad4, p53 and E-cadherin
Comparator
Mouse intestinal-type gastric cancer and intestinal cancer models
Outcome group
Receptor activity and mechanism · Cancer
Source sentences
Summary
In situ hybridization analysis showed that Tmsb4x is highly expressed in E-cadherin-negative mouse DGC models compared with mouse IGC and intestinal cancer models.
1 context sentence(design, population, supporting numbers)
Summary · context
We functionally screened 30 candidate genes using our mouse DGC models lacking Smad4, p53, and E-cadherin.
This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-3408182405
02LabEndogenous levelEx vivo tissueMechanism
In stomach organoids, E-cadherin deficiency increased Tmsb4x expression via Wnt signaling activation.
In plain wordsIn lab-grown stomach organoids, loss of E-cadherin raised the body's own Tmsb4x gene activity.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseTmsb4x expression after E-cadherin deficiency
Study
mousen: not reported in source
stomach organoids
Outcome group
Receptor activity and mechanism · Cancer
Source sentences
Summary
E-cadherin deficiency also increased Tmsb4x expression in stomach organoids via Wnt signaling activation.
1 context sentence(design, population, supporting numbers)
Summary · context
We functionally screened 30 candidate genes using our mouse DGC models lacking Smad4, p53, and E-cadherin.
This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.
Report a problemFND-3408182406

Studies that did not test the peptide alone4

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).

03AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Efficacy outcome
In mouse diffuse-type gastric cancer models, Tmsb4x enhanced metastasis.
In plain wordsIn mice, the Tmsb4x gene promoted spread of diffuse-type stomach cancer.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseDiffuse-type gastric cancer metastasis
Study
mousen: not reported in source
mouse diffuse-type gastric cancer models lacking Smad4, p53 and E-cadherin
Outcome group
Tumor growth · Cancer
Source sentences
Summary
In particular, Tmsb4x enhanced DGC metastasis and stomach organoid-generated tumor growth in in vivo transplantation models.
1 context sentence(design, population, supporting numbers)
Summary · context
We functionally screened 30 candidate genes using our mouse DGC models lacking Smad4, p53, and E-cadherin.
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).
Report a problemFND-3408182401
04AnimalNot a test of Thymosin beta-4 (human) aloneAnimal study (in vivo)Efficacy outcome
In in vivo transplantation models, Tmsb4x enhanced stomach organoid-generated tumor growth.
In plain wordsIn mice, the Tmsb4x gene promoted growth of tumors from stomach organoids.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseStomach organoid-generated tumor growth
Study
mousen: not reported in source
mouse diffuse-type gastric cancer models lacking Smad4, p53 and E-cadherin
Outcome group
Tumor growth · Cancer
Source sentences
Summary
In particular, Tmsb4x enhanced DGC metastasis and stomach organoid-generated tumor growth in in vivo transplantation models.
1 context sentence(design, population, supporting numbers)
Summary · context
We functionally screened 30 candidate genes using our mouse DGC models lacking Smad4, p53, and E-cadherin.
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).
Report a problemFND-3408182402
05LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Efficacy outcome
Tmsb4x promoted tumor clonogenicity.
In plain wordsIn cells, the Tmsb4x gene promoted the ability of tumor cells to form colonies.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseTumor clonogenicity
Study
n: not reported in source
Outcome group
Tumor growth · Cancer
Source sentences
Summary
Tmsb4x promoted tumor clonogenicity and anoikis resistance.
1 context sentence(design, population, supporting numbers)
Summary · context
We functionally screened 30 candidate genes using our mouse DGC models lacking Smad4, p53, and E-cadherin.
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).
Report a problemFND-3408182403
06LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Efficacy outcome
Tmsb4x promoted anoikis resistance of tumor cells.
In plain wordsIn cells, the Tmsb4x gene helped tumor cells resist a form of cell death after detachment.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseAnoikis resistance
Study
n: not reported in source
Outcome group
Tumor growth · Cancer
Source sentences
Summary
Tmsb4x promoted tumor clonogenicity and anoikis resistance.
1 context sentence(design, population, supporting numbers)
Summary · context
We functionally screened 30 candidate genes using our mouse DGC models lacking Smad4, p53, and E-cadherin.
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).
Report a problemFND-3408182404

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.

Version 2Current
13 Oct 2026, 01:52 UTC
Study results updated
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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