LncRNA-PVT1 promotes pancreatic cancer cells proliferation and migration through acting as a molecular sponge to regulate miR-448

2017 ◽  
Vol 233 (5) ◽  
pp. 4044-4055 ◽  
Author(s):  
Liang Zhao ◽  
Hongru Kong ◽  
Hongwei Sun ◽  
Zongjing Chen ◽  
Bicheng Chen ◽  
...  
Pancreas ◽  
2016 ◽  
Vol 45 (9) ◽  
pp. 1263-1271 ◽  
Author(s):  
Hui Feng ◽  
Yalei Wang ◽  
Jiaojiao Su ◽  
Hongwei Liang ◽  
Chen-Yu Zhang ◽  
...  

2020 ◽  
Author(s):  
Pingping Ge ◽  
Dong Fan ◽  
Lei He ◽  
Qiong Wu ◽  
Jin Sun ◽  
...  

Abstract Background: Methyltransferase-like 3(METTL3)-mediated N6-methyladenosine (m6A) modification has been reported to regulate microRNAs maturation. Here, the study was designed to investigate the regulatory effect of m6A-dependent miRNA maturation on pancreatic cancer progression which is still limited before.Results: We found that METTL3 significantly upregulated in the pancreatic tumor tissues. Overexpression of METTL3 promoted cancer cell proliferation and migration in vitro and tumor progression in vivo. METTL3-mediated m6A modification facilitated miR-196a maturation in pancreatic cancer cells, and miR-196a increased the proliferation and migration of cancer cells in vitro. Luciferase reporter assay verified that cytoplasmic polyadenylation element binding protein 3 (CPEB3) was a direct target gene of miR-196a. In vivo studies proved that overexpression of miR-196a inhibited the anti-tumor effect of knockdown of METTL3, and overexpression of CPEB3 inhibited the miR-196a-enhanced tumor progression. Conclusions: We identified that METTL3 was upregulated in pancreatic cancer, leading to the upregulation of miR-196a, resulting in the downregulation of CPEB3, which promoted the pancreatic tumor progression. We first demonstrated that CPEB3 was a tumor suppressor gene in pancreatic cancer, and the METTL3 regulated miR-196a/CPEB3 axis may be a therapeutic target for pancreatic cancer therapy.


2013 ◽  
Vol 24 ◽  
pp. iv49
Author(s):  
Stephanie Booy ◽  
Casper Van Eijck ◽  
Peter Van Koetsveld ◽  
Fadime Dogan ◽  
Joop Janssen ◽  
...  

2020 ◽  
Vol 21 (20) ◽  
pp. 7723
Author(s):  
Priyanka Swami ◽  
Swetha Thiyagarajan ◽  
Arianna Vidger ◽  
Venkata S. K. Indurthi ◽  
Stefan W. Vetter ◽  
...  

The receptor for advanced glycation end products (RAGE) contributes to many cellular aspects of pancreatic cancer including cell proliferation, migration, and survival. Studies have shown that RAGE activation by its ligands promotes pancreatic tumor growth by stimulating both cell proliferation and migration. In this study, we investigated the effect of RAGE up-regulation on the proliferation and migration of the human pancreatic cancer Panc-1 cell-line. We show that moderate overexpression of RAGE in Panc-1 cells results in increased cell proliferation, but decreased cell migration. The observed cellular changes were confirmed to be RAGE-specific and reversible by using RAGE-specific siRNAs and the small molecule RAGE inhibitor FPS-ZM1. At the molecular level, we show that RAGE up-regulation was associated with decreased activity of FAK, Akt, Erk1/2, and NF-κB signaling pathways and greatly reduced levels of α2 and β1 integrin expression, which is in agreement with the observed decreases in cell migration. We also demonstrate that RAGE up-regulation changes the expression of key molecular markers of epithelial-to-mesenchymal transition (EMT). Our results suggest that in the absence of stimulation by external ligands, RAGE up-regulation can differently modulate cell proliferation and migration in pancreatic cancer cells and regulates partly EMT.


2016 ◽  
Vol 12 (4) ◽  
pp. 2761-2765 ◽  
Author(s):  
Wen Zheng ◽  
Shiliu Lu ◽  
Haolei Cai ◽  
Muxing Kang ◽  
Wenjie Qin ◽  
...  

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