Death-Associated Protein Kinase 1 Inhibits Progression of Thyroid Cancer by Regulating Stem Cell Markers

Mi-Hyeon You1, Woo Kyung Lee2, Meihua Jin1

  • 1Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, Korea.

Cells
|November 27, 2021
PubMed

Insights

Death-associated protein kinase 1 (DAPK1) plays a crucial role in thyroid cancer progression. Inhibiting DAPK1 promotes cancer cell stemness and proliferation, while its overexpression suppresses these effects.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Metastatic reprogramming is key to cancer spread, yet its mechanisms remain unclear.
  • The role of death-associated protein kinase 1 (DAPK1) in thyroid cancer progression requires further investigation.

Purpose of the Study:

  • To elucidate the function of DAPK1 in thyroid cancer.
  • To determine DAPK1's impact on cancer cell proliferation, invasion, and stemness.

Main Methods:

  • DAPK1 was knocked down (KD) or overexpressed in human thyroid cancer cell lines (8505C, KTC-1, MDA-T32, BCPAP).
  • Cell proliferation, colony formation, invasion, and tumorsphere formation assays were performed.
  • Expression of stem cell markers (OCT4, Sox2, KLF4, Nanog) and β-catenin pathways were analyzed.

Main Results:

  • DAPK1 KD increased proliferation, colony formation, and tumorsphere formation.
  • DAPK1 overexpression inhibited cancer cell invasion and tumorsphere formation.
  • DAPK1 modulated stem cell marker expression, potentially via β-catenin inhibition, correlating with advanced thyroid cancer stages.

Conclusions:

  • DAPK1 acts as a tumor suppressor in thyroid cancer by inhibiting stemness and metastatic potential.
  • DAPK1 expression levels are linked to thyroid cancer stage, stemness index, and patient survival.

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