ArticleMolecular medicine reports2015
Thymosin β4 promotes hepatoblastoma metastasis via the induction of epithelial-mesenchymal transition.
Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Hepatoblastoma: From Molecular Mechanisms to Therapeutic Strategies.Current oncology (Toronto, Ont.) · 2025Review
- MYBL2 accelerates epithelial-mesenchymal transition and hepatoblastoma metastasis via the Smad/SNAI1 pathway.American journal of cancer research · 2022Article
- Bioengineering strategies to control epithelial-to-mesenchymal transition for studies of cardiac development and disease.APL bioengineering · 2021Review
- Di-(2-ethylhexyl) phthalate-induced tumor growth is regulated by primary cilium formation via the axis of HInternational journal of medical sciences · 2021Article
- Cytoskeletal Remodeling in Cancer.Biology · 2020Review
- Wnt/β-catenin signaling as a useful therapeutic target in hepatoblastoma.Bioscience reports · 2019Review
- The Emerging Roles of Cancer Stem Cells and Wnt/Beta-Catenin Signaling in Hepatoblastoma.Cancers · 2019Review
- Adipose-Derived Mesenchymal Stem Cells Enhance Ovarian Cancer Growth and Metastasis by Increasing Thymosin Beta 4X-Linked Expression.Stem cells international · 2019Article
- Thymosin β4 Regulates Focal Adhesion Formation in Human Melanoma Cells and Affects Their Migration and Invasion.Frontiers in cell and developmental biology · 2019Article
- TMSB10 promotes migration and invasion of cancer cells and is a novel prognostic marker for renal cell carcinoma.International journal of clinical and experimental pathology · 2019Article
- Ratiometric Mass Spectrometry for Cell Identification and Quantitation Using Intracellular "Dual-Biomarkers".Scientific reports · 2017Article
- Article
- Global Proteomics-based Identification and Validation of Thymosin Beta-4 X-Linked as a Prognostic Marker for Head and Neck Squamous Cell Carcinoma.Scientific reports · 2017Article
- "Stealth dissemination" of macrophage-tumor cell fusions cultured from blood of patients with pancreatic ductal adenocarcinoma.PloS one · 2017Article
- Potential role of thymosin Beta 4 in liver fibrosis.International journal of molecular sciences · 2015Review
- Glutathione depletion triggers actin cytoskeleton changes via actin-binding proteins.Genetics and molecular biologyArticle
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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