SEMA3C promotes thyroid cancer via the Wnt/β-catenin pathway
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View abstract on PubMed
Summary
This summary is machine-generated.Semaphorin 3C (SEMA3C) promotes thyroid cancer progression by enhancing cell migration, invasion, and stemness. This effect is mediated by the Wnt/β-catenin pathway, highlighting SEMA3C as a potential therapeutic target.
Area Of Science
- Oncology
- Molecular Biology
- Cell Biology
Background
- Semaphorin 3C (SEMA3C) is implicated in various cancers, but its function in thyroid cancer is uncharacterized.
- Understanding SEMA3C's role is crucial for developing targeted therapies for thyroid malignancies.
Purpose Of The Study
- To investigate the role and underlying mechanisms of Semaphorin 3C (SEMA3C) in thyroid cancer progression.
- To elucidate the involvement of the Wnt/β-catenin pathway in SEMA3C-mediated thyroid cancer development.
Main Methods
- SEMA3C was overexpressed or knocked down in thyroid cancer cell lines (BCPAP, IHH-4).
- Cell migration, invasion, stemness, and epithelial-mesenchymal transition (EMT) were assessed.
- In vivo tumor growth and metastasis models were utilized.
- Wnt/β-catenin pathway activity was evaluated using Dickkopf-1 (DKK1) treatment and β-catenin nuclear translocation assays.
- The upstream regulation of SEMA3C by E1A binding protein P300 (P300) and histone acetylation (H3K27ac) was examined.
Main Results
- SEMA3C overexpression promoted thyroid cancer cell migration, invasion, and EMT.
- SEMA3C enhanced tumor cell stemness and accelerated tumor growth and metastasis in vivo.
- SEMA3C upregulated β-catenin nuclear translocation, indicating Wnt/β-catenin pathway activation.
- Inhibition of the Wnt/β-catenin pathway with DKK1 reversed the pro-tumorigenic effects of SEMA3C.
- P300 was identified as an upstream regulator, increasing SEMA3C transcription via H3K27ac.
Conclusions
- SEMA3C acts as a tumor promoter in thyroid cancer by driving cell migration, invasion, stemness, and metastasis.
- The Wnt/β-catenin pathway is a critical downstream mediator of SEMA3C's oncogenic functions in thyroid cancer.
- P300-mediated transcriptional activation of SEMA3C represents a key regulatory mechanism in thyroid tumorigenesis.
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