ArticleCell death & disease2022
TGF-β induces GBM mesenchymal transition through upregulation of CLDN4 and nuclear translocation to activate TNF-α/NF-κB signal pathway.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 53 citations in OpenAlex.
- Article
- Claudin proteins as emerging therapeutic targets for solid tumours.Nature reviews. Cancer · 2026Review
- Claudins proteins in brain tumors: expression patterns and therapeutic target.Biochemia medica · 2026Review
- CSRP2 modulates PDGFRA/PI3K/AKT signaling via PRC1 components in glioma.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Glioportal: a comprehensive transcriptomic resource unveiling ligand-mediated mesenchymal transition in glioblastoma.Neuro-oncology · 2025Article
- Cyclooxygenase-2 as a potential therapeutic target in the treatment of chemoresistant glioblastomas.Medical oncology (Northwood, London, England) · 2025Review
- Harnessing the role of transforming growth factor-β in glioblastoma: a focus on phytochemicals.Medical oncology (Northwood, London, England) · 2025Review
- A Multi-Layered Atlas of Spatial Regulatory Programs and Therapeutic Vulnerabilities in Glioblastoma.bioRxiv : the preprint server for biology · 2025Article
- Emerging Chemotherapy Targets: Insights from Advances in Glioma Treatment.Biomedicines · 2025Review
- Assessing the diagnostic, prognostic, and therapeutic potential of the somatostatin/cortistatin system in glioblastoma.Cellular and molecular life sciences : CMLS · 2025Article
- RBM24 Suppresses the Tumorigenesis of Glioblastoma by Stabilizing LATS1 mRNA.Biochemical genetics · 2025Article
- Sesquiterpene Lactones as Promising Anti-Glioblastoma Drug Candidates Exerting Complex Effects on Glioblastoma Cell Viability and Proneural-Mesenchymal Transition.Biomedicines · 2025Review
- Tight junction proteins in glial tumors development and progression.Frontiers in cellular neuroscience · 2025Review
- Interactions between glioblastoma and myeloid cells.Frontiers in cell and developmental biology · 2025Review
- A Gene Signature Developed Based on Reactive Oxygen Species to Predict the Metabolism, Immunity, Mutational Status, and Prognostic Survival for Glioblastoma.Current medicinal chemistry · 2025Article
- Armored bicistronic CAR T cells with dominant-negative TGF-β receptor II to overcome resistance in glioblastoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Accurate estimation of pathway activity in single cells for clustering and differential analysis.Genome research · 2024Article
- Humanin activates integrin αV-TGFβ axis and leads to glioblastoma progression.Cell death & disease · 2024Article
- Dissecting TGF-β-induced glioblastoma invasion with engineered hyaluronic acid hydrogels.APL bioengineering · 2024Article
- Comprehensive understanding of glioblastoma molecular phenotypes: classification, characteristics, and transition.Cancer biology & medicine · 2024Review
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma (GBM) is the most common and aggressive primary malignant brain tumor. The unregulated expression of Claudin-4 (CLDN4) plays an important role in tumor progression. However, the biological role of CLDN4 in GBM is still unknown. This study aimed to determine whether CLDN4 mediates glioma malignant progression, if so, it would further explore the molecular mechanisms of carcinogenesis. Our results revealed that CLDN4 was significantly upregulated in glioma specimens and cells. The inhibition of CLND4 expression could inhibit mesenchymal transformation, cell invasion, cell migration and tumor growth in vitro and in vivo. Moreover, combined with in vitro analysis, we found that CLDN4 can modulate tumor necrosis factor-α (TNF-α) signal pathway. Meanwhile, we also validated that the transforming growth factor-β (TGF-β) signal pathway can upregulate the expression of CLDN4, and promote the invasion ability of GBM cells. Conversely, TGF-β signal pathway inhibitor ITD-1 can downregulate the expression of CLDN4, and inhibit the invasion ability of GBM cells. Furthermore, we found that TGF-β can promote the nuclear translocation of CLDN4. In summary, our findings indicated that the TGF-β/CLDN4/TNF-α/NF-κB signal axis plays a key role in the biological progression of glioma. Disrupting the function of this signal axis may represent a new treatment strategy for patients with GBM.
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