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Related Experiment Videos

FOXD3 regulates anaplastic thyroid cancer progression.

Huabin Yin1, Tong Meng1, Lei Zhou2

  • 1Department of Orthopedics, Shanghai Bone Tumor Institute, Shanghai General Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, PR China.

Oncotarget
|April 22, 2017
PubMed
Summary

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Forkhead box D3 (FOXD3) acts as a tumor suppressor in anaplastic thyroid cancer (ATC). Lowering FOXD3 expression promotes cancer invasiveness and tumor growth, suggesting FOXD3 as a potential therapeutic target for ATC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Anaplastic thyroid cancer (ATC) is an aggressive malignancy with a poor prognosis.
  • The transcription factor Forkhead box D3 (FOXD3) has been implicated in various cancers.
  • The specific role of FOXD3 in ATC pathogenesis requires further investigation.

Purpose of the Study:

  • To investigate the antitumorigenic role of FOXD3 in anaplastic thyroid cancer.
  • To determine the effect of FOXD3 expression levels on ATC cell behavior and signaling pathways.
  • To assess the clinical relevance of FOXD3 in human ATC samples.

Main Methods:

  • Comparison of FOXD3 expression in ATC cell lines (SW1736, K18) and normal thyroid cells (Nthy-ori-3-1).
  • Assessment of invasiveness, epithelial-to-mesenchymal transition (EMT), and apoptosis following FOXD3 manipulation.
Keywords:
FOXD3MAPK/ERK signal pathwayhuman anaplastic thyroid cancermetastasis

Related Experiment Videos

  • Analysis of MAPK/ERK signaling pathway components (p-ERK) and E-cadherin levels.
  • Xenograft tumor models in mice to evaluate the in vivo effect of FOXD3 silencing.
  • Examination of FOXD3 and p-ERK expression in human ATC and normal thyroid tissues.

    • Main Results:

    • ATC cell lines exhibited significantly lower FOXD3 expression compared to normal thyroid cells.
    • FOXD3 downregulation promoted invasiveness and EMT while reducing apoptosis in ATC cells.
    • FOXD3 silencing led to increased p-ERK levels, indicating negative regulation of the MAPK/ERK pathway.
    • In vivo, FOXD3 silencing in SW1736 xenografts resulted in larger tumors with elevated p-ERK and reduced E-cadherin.
    • Human ATC samples showed decreased FOXD3 and increased p-ERK levels relative to normal thyroid tissue.

    Conclusions:

    • FOXD3 functions as a tumor suppressor in anaplastic thyroid cancer.
    • FOXD3 downregulation contributes to ATC progression by promoting invasiveness and activating MAPK/ERK signaling.
    • FOXD3 represents a potential therapeutic target for clinical intervention in anaplastic thyroid cancer.