NUSAP1 knockdown inhibits cell growth and metastasis of non‐small‐cell lung cancer through regulating BTG2/PI3K/Akt signaling

2019 ◽  
Vol 235 (4) ◽  
pp. 3886-3893 ◽  
Author(s):  
ZheYuan Xu ◽  
Yang Wang ◽  
Jian Xiong ◽  
FengXian Cui ◽  
Lan Wang ◽  
...  
2021 ◽  
pp. 1-7
Author(s):  
Xiaoyan Zhang ◽  
Hongjun Zhang ◽  
Gangqiang Qi ◽  
Xing Gu ◽  
Yanjun Zhao ◽  
...  

2017 ◽  
Vol 18 (6) ◽  
pp. 860 ◽  
Author(s):  
Yuelei Jin ◽  
Huifang Zhu ◽  
Wei Cai ◽  
Xiaoyan Fan ◽  
Yitao Wang ◽  
...  

Author(s):  
Dandan Li ◽  
Changjun He ◽  
Junfeng Wang ◽  
Yanbo Wang ◽  
Jianlong Bu ◽  
...  

Many studies have shown that downregulation of miR-138 occurs in a variety of cancers including non-small cell lung cancer (NSCLC). However, the precise mechanisms of miR-138 in NSCLC have not been well clarified. In this study, we investigated the biological functions and molecular mechanisms of miR-138 in NSCLC cell lines, discussing whether it could turn out to be a therapeutic biomarker of NSCLC in the future. In our study, we found that miR-138 is downregulated in NSCLC tissues and cell lines. Moreover, the low level of miR-138 was associated with increased expression of SOX4 in NSCLC tissues and cell lines. Upregulation of miR-138 significantly inhibited proliferation of NSCLC cells. In addition, invasion and EMT of NSCLC cells were suppressed by overexpression of miR-138. However, downregulation of miR-138 promoted cell growth and metastasis of NSCLC cells. Bioinformatics analysis predicted that SOX4 was a potential target gene of miR-138. Next, luciferase reporter assay confirmed that miR-138 could directly target SOX4. Consistent with the effect of miR-138, downregulation of SOX4 by siRNA inhibited proliferation, invasion, and EMT of NSCLC cells. Overexpression of SOX4 in NSCLC cells partially reversed the effect of miR-138 mimic. In addition, decreased SOX4 expression could increase the level of miR-138 via upregulation of p53. Introduction of miR-138 dramatically inhibited growth, invasion, and EMT of NSCLC cells through a SOX4/p53 feedback loop.


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