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

Sun,Zhuo; Lu,Jinqi; Wu,Muyu; Ouyang,Changli; Xing,Yueping; Hou,Xiancun; Shi,Zhenduo; Wu,Yongping

doi:10.3892/ol.2019.11028

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

Authors:
- Zhuo Sun
- Jinqi Lu
- Muyu Wu
- Changli Ouyang
- Yueping Xing
- Xiancun Hou
- Zhenduo Shi
- Yongping Wu
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Affiliations: Department of Pathology, Laboratory of Clinical and Experimental Pathology, Xuzhou Medical University, Xuzhou, Jiangsu 221004, P.R. China, Department of Nuclear Medicine, Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu 221000, P.R. China, Department of Urology, Xuzhou Central Hospital, Xuzhou, Jiangsu 221009, P.R. China
Published online on: October 31, 2019 https://doi.org/10.3892/ol.2019.11028
Pages: 6732-6740
Copyright: © Sun et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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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.

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