Retracted : Overexpression of long noncoding RNA SLC26A4‐AS1 inhibits the epithelial–mesenchymal transition via the MAPK pathway in papillary thyroid carcinoma

Papillary thyroid carcinoma (PTC) is recognized as one of the most prevalent types of thyroid cancer with poor prognosis. Long noncoding RNA (lncRNA) has undergone an intensive study for their involvement in tumor treatment. This study intends to unravel the association of lncRNA SLC26A4‐AS1 with PT...

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Bibliographic Details
Published in:Journal of cellular physiology 2020-03, Vol.235 (3), p.2403-2413
Main Authors: Wang, Duo‐Ping, Tang, Xiao‐Zhun, Liang, Quan‐Kun, Zeng, Xian‐Jie, Yang, Jian‐Bo, Xu, Jian
Format: Article
Language:English
Subjects:
Apoptosis
Cancer
Cell adhesion & migration
Cell migration
Deactivation
Extracellular signal-regulated kinase
Inactivation
Kinases
MAP kinase
Mesenchyme
p53 Protein
Papillary thyroid carcinoma
Phosphates
Protein kinase
Ribonucleic acid
RNA
Thyroid
Thyroid cancer
Transfection
Tumors
Vimentin
Xenografts
Xenotransplantation
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Summary:Papillary thyroid carcinoma (PTC) is recognized as one of the most prevalent types of thyroid cancer with poor prognosis. Long noncoding RNA (lncRNA) has undergone an intensive study for their involvement in tumor treatment. This study intends to unravel the association of lncRNA SLC26A4‐AS1 with PTC. Initially, PTC‐related expression profiling data (GSE33630) was utilized to screen differentially expressed lncRNAs in PTC and the underlying mechanisms involved with the mitogen‐activated protein kinase (MAPK) pathway. Moreover, PTC tumor tissues and paracancerous tissues were arranged to determine expressions of TP53, SLC26A4‐AS1, and genes related to epithelial–mesenchymal transition (EMT) and the MAPK pathway. Furthermore, SLC26A4‐AS1 was overexpressed or underexpressed and JNK was underexpressed through cell transfection to examine the effect of SLC26A4‐AS1 on PTC via MAPK pathway. Besides, tumor formation in nude mice was used to verify the fore experiment. LncRNA SLC26A4‐AS1 regulating TP53 had the potential to participate in PTC by regulating the MAPK pathway. SLC26A4‐AS1 was expressed poorly in PTC. Notably, SLC26A4‐AS1 elevated E‐cadherin expression while it reduced that of ERK and Vimentin. In addition, the overexpression of SLC26A4‐AS1 inactivated the MAPK pathway by promoting TP53 and decreased cell migration, proliferation, and invasion. In addition to all these effects, the overexpression of SLC26A4‐AS1 promoted apoptosis of TPC‐1 cells. Additionally, the overexpression of lncRNA SLC26A4‐AS1 reduced xenograft tumor volume in nude mice. Furthermore, the effect of SLC26A4‐AS1 overexpression was found to be promoted after the MAPK pathway inactivation. Taken together, the overexpression of lncRNA SLC26A4‐AS1 coffered anti‐oncogenic effects on PTC through the inactivation of the MAPK pathway.
ISSN:0021-9541
1097-4652
DOI:10.1002/jcp.29145