Wnt信号通路
生物
上皮-间质转换
转染
癌症研究
免疫印迹
信号转导
连环素
甲状腺癌
细胞生物学
细胞生长
活力测定
细胞凋亡
细胞培养
下调和上调
甲状腺
内分泌学
基因
生物化学
遗传学
作者
Jijun Zhong,Rong Lin,Guoyu Wang,Lizhong Lin,Sihan Ruan,Weiping Liu
出处
期刊:Tissue & Cell
[Elsevier]
日期:2022-04-01
卷期号:75: 101739-101739
被引量:1
标识
DOI:10.1016/j.tice.2022.101739
摘要
Papillary thyroid carcinoma (PTC) is the common endocrine malignancy. Kv channel interacting protein 3 (KCNIP3) has been investigated in a variety of diseases, but its role and underlying mechanism in PTC are not fully delineated. Based on this, this study mainly explored the possible mechanism of KCNIP3 in PTC.KCNIP3 expression in PTC tissues was analyzed by ENCORI and validated by quantitative real-time PCR (qRT-PCR). KCNIP3 overexpression (oe-KCNIP3) or KCNIP3 silence (si-KCNIP3) was transfected into IHH4 and FTC-133 cells, respectively. Then cell biological behaviors were detected by cell function assays. The expressions of epithelial-mesenchymal transition (EMT)- and Wnt/β-catenin pathway-related proteins were quantified by qRT-PCR and western blot. Lastly, IHH4 cells were treated with LiCl and the above assays were performed again.The expression of KCNIP3 was decreased in PTC. After transfection, oe-KCNIP3 inhibited the PTC cell viability, cloning, migration and invasion but promoted apoptosis, and meanwhile, oe-KCNIP3 reduced the EMT and Wnt pathway activation. In contrast, si-KCNIP3 had the opposite effect. Moreover, LiCl, a Wnt signaling pathway activator, could reverse the above effects of oe-KCNIP3.KCNIP3 might play an anticarcinogenic role in PTC via inhibiting the activation of Wnt/β-catenin signaling pathway.
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