Thymosin β4 promotes hepatoblastoma metastasis via the induction of epithelial-mesenchymal transition.

Fu X, Cui P, Chen F, Xu J, Gong L, Jiang L, Zhang D, Xiao Y

Molecular medicine reports16 Feb 2015Cited by 21 (Europe PMC)

PMID25695679PMCIDPMC4438935DOI10.3892/mmr.2015.3359PepBankPUB-25695679

Summary

Hepatoblastoma (HB) is the most common malignant hepatic tumor in children and complete surgical resection offers the highest possibility for cure in this disease. Tumor metastasis is the principle obstacle to the development of efficient treatments for patients with HB. The present study aimed to measure the expression levels of thymosin β4 (Tβ4) in liver samples from patients with HB and to investigate the involvement of Tβ4 in HB metastasis. The expression of Tβ4 was significantly higher in liver samples from patients with metastatic HB and in the HepG2 metastatic HB cell line, compared with that in adjacent healthy liver samples and in the L02 healthy hepatic cell line. By contrast, the expression levels of epithelial-cadherin (E-cadherin) and cytosolic accumulation of β-catenin, the two most prominent markers involved in epithelial-mesenchymal transition (EMT), were reduced in liver specimens from patients with metastatic HB compared with that of healthy adjacent control tissue. HepG2 cells were transfected with small interfering-RNA in order to downregulate Tβ4 gene expression. This resulted in a reduced cell migratory capacity compared with control cells. Tβ4 gene expression knockdown significantly inhibited transforming growth factor β1-mediated-EMT in vitro by upregulating the expression of E-cadherin. The results of the present study suggested that Tβ4 may promote HB metastasis via the induction of EMT, and that Tβ4 may therefore be a target for the development of novel treatments for patients with HB.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

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.

01HumanEndogenous levelObservational studyOther
In patients with metastatic hepatoblastoma, expression of the body's own Tβ4 was higher in liver samples than in adjacent healthy liver.
In plain wordsIn patients with metastatic liver cancer, tumor samples had more of the body's own Tβ4 than nearby healthy liver.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseTβ4 expression in metastatic hepatoblastoma liver samples
Study
n: not reported in source
Liver samples from patients with hepatoblastoma
Comparator
Adjacent healthy liver samples
Outcome group
Tumor growth · Cancer
Source sentences
Summary
The expression of Tβ4 was significantly higher in liver samples from patients with metastatic HB and in the HepG2 metastatic HB cell line, compared with that in adjacent healthy liver samples and in the L02 healthy hepatic cell line.
1 context sentence(design, population, supporting numbers)
Summary · context
The present study aimed to measure the expression levels of thymosin β4 (Tβ4) in liver samples from patients with HB and to investigate the involvement of Tβ4 in HB metastasis.
This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.
Show in the study text Report a problemFND-2569567901
02LabEndogenous levelIn vitro (cells)Other
In the HepG2 metastatic hepatoblastoma cell line, expression of the body's own Tβ4 was higher than in the L02 healthy hepatic cell line.
In plain wordsIn lab cells, a liver cancer cell line had more of its own Tβ4 than a healthy liver cell line.
Peptide
Thymosin beta-4 (human)
Outcome
IncreaseTβ4 expression in HepG2 cells
Study
humann: not reported in source
HepG2 metastatic HB cell line
Comparator
L02 healthy hepatic cell line
Outcome group
Tumor growth · Cancer
Source sentences
Summary
The expression of Tβ4 was significantly higher in liver samples from patients with metastatic HB and in the HepG2 metastatic HB cell line, compared with that in adjacent healthy liver samples and in the L02 healthy hepatic cell line.
This result measures the body's own Thymosin beta-4 (human). Nobody was given the peptide. It is not evidence about taking it.
Show in the study text Report a problemFND-2569567902

Studies that did not test the peptide alone2

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).

03LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism
In HepG2 cells, Tβ4 siRNA knockdown reduced cell migratory capacity compared with control cells.
In plain wordsIn lab cells, lowering the cells' own Tβ4 reduced their ability to migrate compared with control cells.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseCell migratory capacity after Tβ4 knockdown
Study
humann: not reported in source
HepG2 cells with Tβ4 siRNA
Comparator
Control cells
Outcome group
Tumor growth · Cancer
Source sentences
Summary
HepG2 cells were transfected with small interfering-RNA in order to downregulate Tβ4 gene expression. This resulted in a reduced cell migratory capacity compared with control 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).
Show in the study text Report a problemFND-2569567903
04LabNot a test of Thymosin beta-4 (human) aloneIn vitro (cells)Mechanism
In HepG2 cells, Tβ4 knockdown significantly inhibited TGF-β1-mediated EMT by upregulating E-cadherin expression.
In plain wordsIn lab cells, lowering the cells' own Tβ4 blocked a change linked to cancer spread and raised E-cadherin.
Peptide
Thymosin beta-4 (human)
Outcome
DecreaseTGF-β1-mediated EMT after Tβ4 knockdown
Study
humann: not reported in source
HepG2 cells with Tβ4 siRNA, TGF-β1-induced EMT
Outcome group
Tumor growth · Cancer
Source sentences
Summary
Tβ4 gene expression knockdown significantly inhibited transforming growth factor β1-mediated-EMT in vitro by upregulating the expression of 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).
Show in the study text Report a problemFND-2569567904

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

Version history

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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

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