MicroRNA-520a-3p suppresses epithelial-mesenchymal transition, invasion, and migration of papillary thyroid carcinoma cells via the JAK1-mediated JAK/STAT signaling pathway (Retracted article. See vol. 237, pg. 2597, 2022)
MicroRNA-520a-3p suppresses epithelial-mesenchymal transition, invasion, and migration of papillary thyroid carcinoma cells via the JAK1-mediated JAK/STAT signaling pathway (Retracted article. See vol. 237, pg. 2597, 2022)
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DOI：
10.1002/jcp.27199
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发表时间：
2019-04-01
影响因子：
5.6
通讯作者：
Fu, Yi-Li
中科院分区：
文献类型：
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作者：
Bi, Chang-Long;Zhang, Ying-Qi;Fu, Yi-Li
甲状腺乳头状癌（PTC）是甲状腺癌的一种，常表现为上皮间质转化（EMT）。microRNAs（miRNAs）与PTC的发生有关。因此，本研究旨在通过靶向JAK 1来确定microRNA-520 a-3 p（miR-520 a-3 p）通过JAK/STAT信号通路在PTC中的作用。收集137例PTC患者的PTC及正常甲状腺组织。首先，确定miR-520 a-3 p、JAK 1、JAK 2、STAT 3、E-cadherin和vimentin在PTC中的表达模式。预测并分析miR-520 a-3 p与JAK 1的关系。并将一系列miR-520 a-3 p模拟物或抑制剂，或siRNA JAK 1导入PTC细胞，检测miR-520 a-3 p对PTC细胞活力、迁移、侵袭、细胞周期、凋亡和EMT的影响。同时，我们还研究了miR-520 a-3 p和JAK 1对JAK/STAT信号通路的调控作用。PTC组织中JAK 1、JAK 2、STAT 3和vimentin的表达增加，而miR-520 a-3 p和E-cadherin的表达减少。JAK 1受miR-520 a-3 p负调节。在功能上，通过下调JAK 1上调miR-520 a-3 p来阻止EMT诱导。当在PTC细胞中上调miR-520 a-3 p或沉默JAK 1时，PTC细胞活力、迁移和侵袭受到抑制，而细胞凋亡促进细胞停滞在G1期，表明miR-520 a-3 p通过下调JAK 1阻止PTC进展。此外，miR-520 a-3 p升高或JAK 1抑制使JAK/STAT信号通路失活。总体而言，miR-520 a-3 p通过下调PTC中的JAK 1使JAK/STAT信号通路失活来预防癌症进展。
Papillary thyroid cancer (PTC) is a kind of thyroid cancer and frequently presents with epithelial-mesenchymal transition (EMT). MicroRNAs (miRNAs) were previously reported to be associated with PTC. Thus, this study aims to define the role of microRNA-520a-3p (miR-520a-3p) in PTC through the JAK/STAT signaling pathway by targeting JAK1. The PTC and normal thyroid tissues of 137 PTC patients were collected. First of all, the expression pattern of miR-520a-3p, JAK1, JAK2, STAT3, E-cadherin, and vimentin in PTC was identified. The relationship between miR-520a-3p and JAK1 was predicted and analyzed. And a series of miR-520a-3p mimic or inhibitor, or siRNA JAK1 introduced into PTC cells were applied to examine the effect of miR-520a-3p on PTC cell viability, migration, invasion, cell cycle, apoptosis, and EMT. Meanwhile, the regulatory effect of miR-520a-3p and JAK1 on the JAK/STAT signaling pathway was also determined. The expression of JAK1, JAK2, STAT3, and vimentin increased yet miR-520a-3p and E-cadherin decreased in PTC tissue. JAK1 was negatively regulated by miR-520a-3p. Functionally, EMT induction was prevented by miR-520a-3p upregulation through downregulating JAK1. When upregulating miR-520a-3p or silencing JAK1 in PTC cells, PTC cell viability, migration, and invasion were inhibited yet cell apoptosis promoted with cells arrested at G1 phase, indicating that miR-520a-3p prevented PTC progression by downregulating JAK1. Moreover, miR-520a-3p elevation or JAK1 inhibition inactivated the JAK/STAT signaling pathway. Collectively, miR-520a-3p prevents cancer progression through inactivating the JAK/STAT signaling pathway by downregulating JAK1 in PTC.