Title:Receptor Type Protein Tyrosine Phosphatase Epsilon (PTPRE) Plays an
Oncogenic Role in Thyroid Carcinoma by Activating the AKT and
ERK1/2 Signaling Pathway
Volume: 23
Issue: 6
Author(s): Chen Peng, Chunming Zhang, Wenjie Yu, Le Li, Zhen Zhang, Ting Liu, Yan Zhang, Gaiping Fan*Hui Huangfu*
Affiliation:
- Department of Head and Neck Surgery, Shanxi Province Cancer Hospital, Taiyuan, 030001, China
- Department of
Head and Neck Surgery, Shanxi Hospital Affiliated to Cancer Hospital, Chinese Academy of Medical Sciences, Taiyuan,
030001, China
- Cancer Hospital Affiliated to Shanxi Medical University, Taiyuan, 030001, China
- Otolaryngology Head and Neck Surgery Research Institute, Shanxi Medical University, Taiyuan, 030001, China
- Department of Otolaryngology
Head and Neck Surgery, First Hospital of Shanxi Medical University, Taiyuan, 030001, China
- Shanxi Key
Laboratory of Otorhinolaryngology Head and Neck Cancer, First Hospital of Shanxi Medical University, Taiyuan,
030001, China
Keywords:
PTPRE, thyroid carcinoma, AKT, ERK1/2, EMT, TNM, RT-qPCR.
Abstract:
Background: Thyroid carcinoma (TC) is a common malignant tumor in human and its incidence
has been increasing in recent years. Studies have shown that receptor type protein tyrosine
phosphatase epsilon (PTPRE) is a key regulator of tumorigenesis in cancer progression, but its role in
TC has not been revealed.
Objective: Here, in this work, we explored the essential role of PTPRE in TC progression.
Methods: The expression of PTPRE in TC clinical samples and cell lines was detected by RT-qPCR
and Western blot. Cell proliferation was measured by MTT and cell cycle analysis. Cell migration,
invasion and epithelial-mesenchymal transition (EMT) were analyzed by wound healing, transwell,
and immunofluorescent staining assays. AKT and ERK1/2 signaling pathway related protein level was
analyzed by Western blot.
Results: PTPRE was highly expressed in TC clinical samples and cell lines, especially anaplastic thyroid
carcinoma (ATC). High level of PTPRE was associated with tumor size and TNM stage. Upregulated
PTPRE promoted cell proliferation, and enhanced the migration, invasion and EMT of TC cells,
whereas the knockdown of PTPRE suppressed these behaviors. Importantly, we confirmed that the
AKT and ERK1/2 signaling pathways were activated by PTPRE, reflected by the enhanced protein
level of phosphorylated AKT and ERK1/2.
Conclusion: Accordingly, we indicated that PTPRE plays an oncogenic role in TC progression via
activating the AKT and ERK1/2 signaling pathway. These findings indicated that modulation of
PTPRE expression may as a potential strategy to interfere with the progression of TC.
