KIF3a inhibits TGF-β1-induced epithelial-mesenchymal transition in lung cancer cells

被引:0
|
作者
Shan, Yang-Yang [1 ]
Li, Sheng-Lei [2 ]
机构
[1] Zhengzhou Univ, Affiliated Hosp 5, Dept Geriatr, 3 Zhengzhou Rehabil St, Zhengzhou 450052, Peoples R China
[2] Zhengzhou Univ, Affiliated Hosp 5, Dept Pathol, Zhengzhou 450052, Peoples R China
来源
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE | 2016年 / 9卷 / 02期
关键词
KIF3a; lung cancer; epithelial-mesenchymal transition (EMT); Wnt signaling; TGF-BETA; TUMOR PROGRESSION; CATENIN; EXPRESSION; PROTEINS; INVASIVENESS; PROGNOSIS; CARCINOMA; CADHERIN; PATHWAY;
D O I
暂无
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
KIF3a is a subunit of hetero-trimeric Kinesin-2, a microtubule (MT) plus-end directed motor protein and has been reported to be involved in tumorigenesis. However, the roles of KIF3a in lung cancer remain unknown. Hence, in the present study, we explored the regulatory effects of KIF3a during the transforming growth factor (TGF)-beta 1-induced epithelial-mesenchymal transition (EMT) in lung adenocarcinoma cells. The results showed that KIF3a was downregulated after induction with TGF-beta 1. Overexpression of KIF3a inhibited the TGF-beta 1-induced migration and invasion, as well as EMT phenotype of lung cancer cells. Furthermore, overexpression of KIF3a inhibited the TGF-beta 1-induced the expression of beta-catenin, cyclin D1 and c-myc in A549 cells. Taken together, these results indicate overexpression of KIF3a might inhibit TGF-beta 1-induced EMT by blocking the Wnt signaling in A549 cells, providing potential targets to prevent and/or treat lung cancer cell invasion and metastasis.
引用
收藏
页码:2528 / 2534
页数:7
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