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Stemness is Derived from Thyroid Cancer Cells.

Risheng Ma1, Simon Bonnefond2, Syed A Morshed1

  • 1Thyroid Research Unit, Department of Medicine, Icahn School of Medicine at Mount Sinai and the James J Peters VA Medical Center , New York, NY , USA.

Frontiers in Endocrinology
|August 1, 2014
PubMed
Summary
This summary is machine-generated.

Thyroid cancer stemness arises from epithelial to mesenchymal transition (EMT), not resident stem cells. This process involves dedifferentiation of thyroid cells and can be inhibited by celastrol, suggesting therapeutic potential.

Keywords:
Brafcancer stem cellscelastrolepithelial–mesenchymal transitionthyroglobulinthyroid papillary carcinomathyroid peroxidase

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Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Thyroid cancer development may involve cancer stem cells (CSCs).
  • Epithelial to mesenchymal transition (EMT) confers stem-like properties and is crucial for tumor progression and metastasis.
  • The roles of EMT and stemness in thyroid cancer progression require further investigation.

Purpose of the Study:

  • To investigate the origin of stemness in thyroid papillary cancer.
  • To examine the relationship between EMT and stemness in a murine model of thyroid papillary carcinoma.
  • To evaluate the therapeutic potential of celastrol in inhibiting EMT and stemness.

Main Methods:

  • Utilized a murine model with thyroid-specific knock-in of oncogenic Braf (LSL-Braf((V600E))/TPO-Cre).
  • Assessed stemness and EMT markers using qPCR and histochemistry.
  • Investigated EMT induction and inhibition in a derived thyroid cancer cell line (Marca cells).

Main Results:

  • Dedifferentiated thyroid carcinoma tissue showed decreased thyroid-specific genes (Tg, NIS) and increased stemness markers (Oct4, Rex1, CD15, Sox2).
  • Evidence of EMT progression (decreased E-cadherin, increased Snail, Slug, TGF-β, vimentin) alongside CSC-like phenotype.
  • Overexpression of Snail enhanced migration and stemness markers; TGF-β1 induced EMT, which celastrol inhibited.

Conclusions:

  • Stemness in thyroid cancer originates from EMT, not resident stem cells.
  • Neoplastic changes and stemness onset depend on thyroid cell differentiation.
  • Celastrol suppresses TGF-β1-induced EMT in thyroid cancer cells, indicating therapeutic potential.