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NKX2-1 re-expression induces cell death through apoptosis and necrosis in dedifferentiated thyroid carcinoma cells

Yuko Ito1, Fumihiko Furuya2, Katsumi Taki3

  • 1Department of Laboratory Medicine, School of Medicine, Fukushima Medical University, Fukushima, Fukushima, Japan.

Plos One
|November 8, 2021
PubMed

Insights

Re-expressing NK2 homeobox 1 (NKX2-1) in thyroid cancer cells induced cell death through apoptosis and necrosis. This process involves the upregulation of specific genes, particularly Regulator of G protein signaling 4 (RGS4).

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Endocrinology

Background:

  • NK2 homeobox 1 (NKX2-1) is a crucial thyroid transcription factor for thyroid development and function.
  • Reduced NKX2-1 expression correlates with dedifferentiation in thyroid cancer.
  • Mechanisms linking NKX2-1 to thyroid cancer phenotypes remain largely unelucidated.

Purpose of the Study:

  • To investigate the impact of NKX2-1 re-expression on dedifferentiated thyroid cancer cell death.
  • To explore the molecular mechanisms underlying NKX2-1-mediated cell death.

Main Methods:

  • Utilized an adenoviral vector for NKX2-1 re-expression in a human papillary thyroid carcinoma cell line lacking NKX2-1.
  • Assessed cell viability, apoptosis, and necrosis following NKX2-1 transduction.
  • Quantified mRNA expression of Arginase 2 (ARG2), Regulator of G protein signaling 4 (RGS4), and RGS5.
  • Employed siRNA to suppress ARG2, RGS4, and RGS5 expression and evaluated effects on cell death.

Main Results:

  • NKX2-1 re-expression significantly decreased cell viability and induced apoptosis and necrosis.
  • Upregulation of ARG2, RGS4, and RGS5 mRNA was observed in NKX2-1-expressing cells.
  • siRNA-mediated knockdown of RGS4 reduced cell death, apoptosis, and necrosis.

Conclusions:

  • Re-expression of NKX2-1 induces cell death in dedifferentiated thyroid cancer cells via apoptosis and necrosis.
  • The tumor suppressor role of NKX2-1 in thyroid cancer involves the RGS4 pathway.
  • NKX2-1 re-expression presents a potential therapeutic strategy for thyroid cancer.

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