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Updated: Jun 16, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
TMEM252 inhibits epithelial-mesenchymal transition and progression in papillary thyroid carcinoma by regulating
Shuyong Zhang1, Rong Xie1, Liuhuan Wang1
1Department of Thyroid Surgery, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Background:
Papillary thyroid carcinoma (PTC) accounts for about 85% of thyroid cancer cases. Transmembrane protein 252 (TMEM252) is a gene encoding a transmembrane protein that has only been reported to be associated with triple-negative breast cancer. Herein, we first elucidated the physiological roles and possible regulatory proteins of TMEM252 in PTC pathogenesis.
Methods:
Quantitative real-time polymerase chain reaction, western blot, and immunohistochemical analyses were utilized to ascertain the relative TMEM252 expression in PTC and surrounding normal tissues. Functional investigations involved CCK-8 viability assay, EdU incorporation assay for proliferation, transwell assays for migration and invasion, and an in vivo tumor development assessment to evaluate the TMEM252-mediated regulation of tumor formation.
Results:
Our results first revealed diminished TMEM252 transcript and protein expressions in PTC tissues and cell lines. TMEM252 overexpression suppressed cell proliferation through reducing p53, p21, and p16 expression. Conversely, TMEM252 depletion has opposite effects in PTC cells both in vivo. Additionally, the upregulation of TMEM252 demonstrated cell migration and invasion suppression by impeding the epithelial-mesenchymal transition (EMT) process via inhibition of the Notch pathway. Furthermore, overexpression of TMEM252 suppressed tumor growth in vivo.
Conclusion:
Our study elucidates that TMEM252 suppresses PTC progression by modulating the Notch pathway. These findings underscore TMEM252 is a potential therapeutic target in managing PTC.
Insights
Transmembrane protein 252 (TMEM252) suppresses papillary thyroid carcinoma (PTC) progression by inhibiting the Notch pathway. This finding highlights TMEM252 as a potential therapeutic target for PTC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer.
- Transmembrane protein 252 (TMEM252) has not been previously studied in the context of PTC.
- This study investigates the role of TMEM252 in PTC pathogenesis.
Purpose of the Study:
- To elucidate the physiological roles of TMEM252 in PTC.
- To identify potential regulatory proteins of TMEM252 in PTC.
- To explore TMEM252 as a therapeutic target for PTC.
Main Methods:
- Quantitative real-time polymerase chain reaction, western blot, and immunohistochemistry were used to assess TMEM252 expression.
- Functional assays included CCK-8, EdU, and transwell assays to evaluate proliferation, migration, and invasion.
- In vivo tumor development assessments were performed.
Main Results:
- TMEM252 expression was found to be diminished in PTC tissues and cell lines.
- TMEM252 overexpression suppressed PTC cell proliferation, migration, and invasion by inhibiting the epithelial-mesenchymal transition (EMT) and Notch pathway.
- TMEM252 overexpression also suppressed tumor growth in vivo.
Conclusions:
- TMEM252 suppresses PTC progression through modulation of the Notch pathway.
- TMEM252 demonstrates potential as a therapeutic target for PTC management.
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