ArticleBMC cancer2020
A novel TGF-β receptor II mutation (I227T/N236D) promotes aggressive phenotype of oral squamous cell carcinoma via enhanced EGFR signaling.
Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 28 citations in OpenAlex.
- Curcumin and Its Derivatives as Anticancer Agents in Head and Neck Cancer: Molecular Mechanisms and Preclinical Evidence.International journal of molecular sciences · 2026Review
- Aspartame carcinogenic potential revealed through network toxicology and molecular docking insights.Scientific reports · 2024Article
- The paradoxical role of transforming growth factor-β in controlling oral squamous cell carcinoma development.Cancer biomarkers : section A of Disease markers · 2024Review
- Immunotherapy for the Treatment of Squamous Cell Carcinoma: Potential Benefits and Challenges.International journal of molecular sciences · 2022Review
- Targeting TGF-β signal transduction for fibrosis and cancer therapy.Molecular cancer · 2022Review
- Propofol induces apoptosis and ameliorates 5‑fluorouracil resistance in OSCC cells by reducing the expression and secretion of amphiregulin.Molecular medicine reports · 2022Article
- Bioinformatics-based analysis of the association between the A1-chimaerin (Bioengineered · 2021Article
- MYLK4 promotes tumor progression through the activation of epidermal growth factor receptor signaling in osteosarcoma.Journal of experimental & clinical cancer research : CR · 2021Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundTransforming growth factor-β (TGF-β) signaling is a double-edged sword in cancer development and progression. TGF-β signaling plays a tumor suppressive role during the early stages of tumor development but promotes tumor progression in later stages. We have previously identified various mutations of TGF-β receptor II (TβRII) in human oral squamous cell carcinoma (OSCC) samples. In the present study we analyzed I227T/N236D mutation of TβRII, which was detected in the metastatic lymph node of an OSCC patient.
methodsThe effect of I227T/N236D TβRII mutation on transcriptional activities was measured using DR26 cells, which lack functional TβRII. HSC2 human OSCC cells stably expressing wild-type and I227T/N236D mutant TβRII were generated and used to examine the effect of I227T/N236D TβRII mutation on xenograft tumor growth, in vitro cell proliferation, apoptosis, migration, and invasion.
resultsThe I227T/N236D mutation of TβRII upregulated TGF-β signaling and promoted xenograft tumor growth when compared with the wild-type, without affecting the in vitro proliferative capacities. To delineate the differences in proliferative capacities in vivo and in vitro, the apoptotic and survival signals were analyzed following curcumin treatment. Concomitant with apoptotic induction, epidermal growth factor receptor (EGFR) activation was observed upon curcumin treatment, which was further activated in I227T/N236D mutant transfectant cells when compared with wild-type cells. Enhanced EGFR activation correlated with cell survival and apoptotic resistance. Enhanced migratory and invasive capabilities of I227T/N236D mutant cells also depended on EGFR signaling.
conclusionsThese results suggest that enhanced EGFR signaling via upregulated TGF-β signaling shifted the balance toward survival and promoted cell migration and invasion in I227T/N236D mutant cells, elucidating the role of I227T/N236D mutation of TβRII in OSCC progression.
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