scholarly journals PNUTS mediates ionizing radiation-induced CNE-2 nasopharyngeal carcinoma cell migration, invasion, and epithelial–mesenchymal transition via the PI3K/AKT signaling pathway

2019 ◽  
Vol Volume 12 ◽  
pp. 1205-1214 ◽  
Author(s):  
Dan Yu ◽  
Xiang An ◽  
Wanlin Fan ◽  
Xin Wang ◽  
Yuxing He ◽  
...  
Keyword(s):  
Cell Migration ◽  
Nasopharyngeal Carcinoma ◽  
Ionizing Radiation ◽  
Signaling Pathway ◽  
Carcinoma Cell ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Mesenchymal Transition ◽  
Nasopharyngeal Carcinoma Cell ◽  
Radiation Induced

scholarly journals ARHGAP42 promotes cell migration and invasion involving PI3K/Akt signaling pathway in nasopharyngeal carcinoma

2018 ◽  
Vol 7 (8) ◽  
pp. 3862-3874 ◽  
Author(s):  
Qian Hu ◽  
Xiao Lin ◽  
Linxiaoxiao Ding ◽  
Yinduo Zeng ◽  
Danmei Pang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Nasopharyngeal Carcinoma ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Migration And Invasion ◽  
Akt Signaling Pathway ◽  
Cell Migration And Invasion

scholarly journals YBX3 Mediates the Metastasis of Nasopharyngeal Carcinoma via PI3K/AKT Signaling

2021 ◽  
Vol 11 ◽  
Author(s):  
Xiaoqin Fan ◽  
Xina Xie ◽  
Ming Yang ◽  
Yujie Wang ◽  
Hanwei Wu ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Signaling Pathway ◽  
Epithelial To Mesenchymal Transition ◽  
Rna Binding ◽  
Akt Signaling ◽  
Ras Signaling ◽  
Akt Signaling Pathway ◽  
Mesenchymal Transition

The metastasis of nasopharyngeal carcinoma (NPC) is a complex process associated with oncogenic dysfunction, the deciphering of which remains a challenge and requires more in-depth studies. Y-box protein 3 (YBX3) is a DNA/RNA binding protein associated with gene transcription, DNA repair, and the progression of various diseases. However, whether and how YBX3 affects the metastasis of NPC remains unknown. Thus, in this study, we aimed to investigate the role of YBX3 in the metastasis of NPC and determine its underlying mechanism. Interestingly, it was found that the expression of YBX3, which was associated with NPC metastasis, was upregulated in the clinical NPC tissues and cell lines. Moreover, we found that knockdown of YBX3 expression by lentivirus shRNA significantly suppressed NPC cells migration in vitro and metastasis in vivo. Mechanistically, RNA sequencing results suggested that the genes regulated by YBX3 were significantly enriched in cell adhesion molecules, cAMP signaling pathway, calcium signaling pathway, focal adhesion, PI3K/AKT signaling pathway, Ras signaling pathway, Rap1 signaling pathway, NF-κB signaling pathway, and Chemokine signaling pathway. Of these, PI3K/AKT signaling pathway contained the most genes. Accordingly, YBX3 knockdown decreased the activation of PI3K/AKT signaling pathway, thereby inhibit epithelial-to-mesenchymal transition (EMT) and MMP1. These results have demonstrated that YBX3 are involved in the metastasis of NPC through regulating PI3K/AKT signaling pathway, and serve as a potential therapeutic target for patients with NPC.

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