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Updated: Jan 2, 2026

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Published on: August 23, 2014
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.
Abstract:
The incidence of thyroid disorders, which are common endocrine diseases, has rapidly increased in recent years. However, the etiology and pathogenesis of these disorders remain unclear. Phosphatase and tension homolog (PTEN) is a dual-specific phosphatase that is associated with multiple thyroid disorders; however, the role of PTEN in thyroid disorders remains unknown. In the present study, the human thyroid follicular epithelial cell line Nthy-Ori 3-1 was used to determine the role of PTEN in thyroid disorders. PTEN expression was knocked down using a PTEN-specific short hairpin RNA. Western blotting was subsequently used to determine protein expression, the Matrigel tube formation assay and iodide uptake assay were applied for evaluating the morphology and function of thyroid cells. The results showed that PTEN knockdown decreased the protein expression of paired box 8 (PAX8). The morphology and tubular-like growth pattern of thyroid cells were therefore disrupted, and restoration of PAX8 expression reversed these effects. Furthermore, PTEN-knockdown decreased the expression of specific thyroid proteins (thyroglobulin, TG; thyroid peroxidase, TPO; and sodium/iodide symporter, NIS) and inhibited the iodide uptake ability of thyroid cells by downregulating PAX8, suggesting that PTEN deficiency may impair the function of thyroid cells. In conclusion, the present study reported an important function of PTEN in normal thyroid cells and identified the involvement of PAX8. These results may improve understanding of the role of PTEN in the pathogenesis of thyroid disorders.
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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