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Silencing SIX1 inhibits epithelial mesenchymal transition through regulating TGF-β/Smad2/3 signaling pathway in papillary thyroid carcinoma.

Authors
  • Min, Wen-Pu1
  • Wei, Xiao-Feng2
  • 1 Department of Nuclear Medicine, The First People's Hospital of Jingzhou City, The First Affiliated Hospital of Yangtze University, Jingzhou 434000, Hubei Province, China. , (China)
  • 2 Department of Nuclear Medicine, The First People's Hospital of Jingzhou City, The First Affiliated Hospital of Yangtze University, Jingzhou 434000, Hubei Province, China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Auris, nasus, larynx
Publication Date
Jun 01, 2021
Volume
48
Issue
3
Pages
487–495
Identifiers
DOI: 10.1016/j.anl.2020.10.002
PMID: 33077306
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

To investigate the sineoculis homeobox homolog 1 (SIX1) affect the epithelial mesenchymal transition (EMT) in papillary thyroid carcinoma (PTC) through regulating TGF-β/Smad2/3 signaling pathway. The SIX1 expression in cytological specimens, tissues or PTC cell lines was detected by qRT-PCR, western blotting or immunohistochemistry. A series of vitro experiments including flow cytometry, CCK-8, wound-healing and Transwell were used to evaluate the biological characteristics in a PTC cell line (NPA cells), which were divided into Blank, Negative control (NC), SIX1, SIX1-siRNA, LY-364947 (TGF-β/Smad2/3 pathway inhibitor) and SIX1 + LY-364947 groups. TGF-β/Smad2/3 pathway and EMT related protein expression were measured by qRT-PCR and western blotting. SIX1 mRNA expression was increased in cytological specimens from PTC patients as compared with the non-toxic nodular goitre (NTG) patients. Moreover, compared with adjacent normal tissues, expressions of SIX1, N-cadherin and Vimentin were higher while E-cadherin was lower in PTC tissues; and SIX1 was positively correlated with N-cadherin and Vimentin but was negatively correlated with E-cadherin. Furthermore, the SIX1 expression was associated with histopathology, extrathyroidal extension (ETE), lymph node metastasis (LNM), pT stage, TNM stage, and distant metastasis. In addition, the expressions of TGFβ1, p-SMAD2/3, N-cadherin and Vimentin were downregulated in NPA cells after LY-364947 treatment with upregulated E-cadherin, decreased cell proliferation and metastasis, and enhanced cell apoptosis, which was reversed by SIX1 overexpression. Silencing SIX1 can inhibit TGF-β/Smad2/3 pathway, thereby suppressing EMT in PTC, which may be a novel avenue for the treatment of PTC. Copyright © 2020. Published by Elsevier B.V.

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