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F-Box protein 4 inhibits progression of papillary thyroid cancer.

Authors
  • Xu, Min1
  • Wang, Youmin1
  • Chen, Mingwei1
  • Hu, Honglin1
  • Xia, Tongjia1
  • Deng, Datong2
  • 1 Department of Endocrinology, The First Affiliated Hospital of AnHui Medical University, No. 218 Jixi Road, Hefei 230022, Anhui, China. , (China)
  • 2 Department of Endocrinology, The First Affiliated Hospital of AnHui Medical University, No. 218 Jixi Road, Hefei 230022, Anhui, China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Steroids
Publication Date
Feb 01, 2021
Volume
166
Pages
108773–108773
Identifiers
DOI: 10.1016/j.steroids.2020.108773
PMID: 33285173
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

We aimed to investigate the role of F-Box protein 4 (FBXO4) in the progression of papillary thyroid cancer (PTC) and to reveal the underlying signaling pathways responsible for FBXO4 action in PTC. FBXO4 expression was evaluated in tissues from PTC patients as well as in cell lines. Overexpression of FBXO4 was re-introduced into PTC cell line B-CPAP, followed by analysis of cell migration, invasion, apoptosis and epithelial-mesenchymal transition (EMT) marker profile. An in vivo xenograft tumor mouse model was employed to address the role of FBXO4 in tumorigenesis as well. Endogenous FBXO4 was downregulated in PTC patient tissues and cell lines. Upon re-introducing its expression, FBXO4 suppressed migration and invasion and induced apoptosis of PTC cells, as well as inhibited EMT. Using a xenograft tumor mouse model, the pro-apoptotic and anti-EMT functions of FBXO4 are also validated in vivo, resulting in considerably slowed tumor growth rate of inoculated FBXO4-expressing PTC cells. Our results therefore propose the potential therapeutic value of FBXO4 in targeted treatments against PTC. Copyright © 2020 Elsevier Inc. All rights reserved.

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