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首页> 外文期刊>Journal of cellular physiology. >Overexpression of long noncoding RNA SLC26A4-AS1 inhibits the epithelial-mesenchymal transition via the MAPK pathway in papillary thyroid carcinoma
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Overexpression of long noncoding RNA SLC26A4-AS1 inhibits the epithelial-mesenchymal transition via the MAPK pathway in papillary thyroid carcinoma

机译：过度的非编码RNA SLC26A4-AS1抑制epithelial-mesenchymal过渡通过MAPK通路在乳头状甲状腺癌

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摘要

Papillary thyroid carcinoma (PTC) is recognized as one of the most prevalent types of thyroid cancer with poor prognosis. Long noncoding RNA (IncRNA) has undergone an intensive study for their involvement in tumor treatment. This study intends to unravel the association of IncRNA SLC26A4-AS1 with PTC. Initially, PTC-related expression profiling data (GSE33630) was utilized to screen differentially expressed IncRNAs 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 IncRNA 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 IncRNA SLC26A4-AS1 coffered anti-oncogenic effects on PTC through the inactivation of the MAPK pathway.
机译：乳头状甲状腺癌(PTC)被认为是其中一个最普遍类型的甲状腺癌较差的预后。经历了一个深入研究的参与肿瘤的治疗。打算解开IncRNA协会SLC26A4-AS1 PTC(列车自动控制系统)。表达分析数据(GSE33630)是利用筛选差异表达IncRNAs PTC(列车自动控制系统)和所涉及的潜在机制增殖蛋白激酶(MAPK)途径。此外,肿瘤组织和paracancerous PTC(列车自动控制系统)组织安排确定的表达TP53、SLC26A4-AS1和基因有关epithelial-mesenchymal (EMT)和过渡MAPK通路。过表达或underexpressed物通过细胞转染underexpressed检查通过MAPK SLC26A4-AS1对PTC(列车自动控制系统)的影响途径。被用来验证实验。SLC26A4-AS1调节TP53的潜力参与PTC(列车自动控制系统通过调节MAPK途径。值得注意的是,SLC26A4-AS1钙粘蛋白升高表情虽然ERK和减少波形蛋白。SLC26A4-AS1灭活MAPK通路促进TP53、减少细胞迁移,扩散和入侵。这些影响,SLC26A4-AS1的过度提升TPC-1细胞的凋亡。的超表达IncRNA SLC26A4-AS1减少在裸鼠异种移植肿瘤体积。SLC26A4-AS1进行靶向治疗的效果MAPK通路后发现被提升失活。的IncRNA SLC26A4-AS1方格anti-oncogenic对PTC的失活的影响MAPK通路。

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