PTEN-knockdown disrupts the morphology, growth pattern and function of Nthy-Ori 3-1 cells by downregulating PAX8

Zhuo Sun1, Jinqi Lu1,2, Muyu Wu1

  • 1Department of Pathology, Laboratory of Clinical and Experimental Pathology, Xuzhou Medical University, Xuzhou, Jiangsu 221004, P.R. China.

Oncology Letters
|December 7, 2019
PubMed

Insights

Phosphatase and tension homolog (PTEN) deficiency impairs thyroid cell function by reducing paired box 8 (PAX8) expression. This disruption affects thyroid cell morphology and iodide uptake, highlighting PTEN

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Biology

Background:

  • Thyroid disorders are common endocrine diseases with unclear etiology and pathogenesis.
  • Phosphatase and tension homolog (PTEN) is implicated in various thyroid disorders, but its specific role is unknown.

Purpose of the Study:

  • To investigate the role of PTEN in thyroid follicular epithelial cells.
  • To elucidate the molecular mechanisms underlying PTEN's function in thyroid disorders.

Main Methods:

  • Utilized the Nthy-Ori 3-1 human thyroid follicular epithelial cell line.
  • Performed PTEN knockdown using short hairpin RNA (shRNA).
  • Assessed protein expression via Western blotting, cell morphology and function using Matrigel tube formation and iodide uptake assays.

Main Results:

  • PTEN knockdown decreased paired box 8 (PAX8) protein expression.
  • Disrupted thyroid cell morphology and tubular-like growth, which was reversed by restoring PAX8.
  • Reduced expression of thyroglobulin (TG), thyroid peroxidase (TPO), and sodium/iodide symporter (NIS), impairing iodide uptake via PAX8 downregulation.

Conclusions:

  • PTEN plays a crucial role in maintaining normal thyroid cell function.
  • PTEN deficiency impairs thyroid function by downregulating PAX8, affecting cell morphology and iodide uptake.
  • These findings contribute to understanding PTEN's role in thyroid disorder pathogenesis.

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