Interleukin‐1β/nuclear factor‐κB signaling promotes osteosarcoma cell growth through the microRNA‐181b/phosphatase and tensin homolog axis

2018 ◽  
Vol 120 (2) ◽  
pp. 1763-1772 ◽  
Author(s):  
Weiguo Wang ◽  
Zhengguang Wang ◽  
Shijie Chen ◽  
Xiaofang Zang ◽  
Jinglei Miao
2001 ◽  
Vol 280 (6) ◽  
pp. G1296-G1304 ◽  
Author(s):  
Satoru Takahashi ◽  
Takuya Fujita ◽  
Akira Yamamoto

We investigated the role of nuclear factor-κB (NF-κB) in gastric ulcer healing in rats. NF-κB was activated in ulcerated tissue but not in normal mucosa, and the level of the activation was decreased with ulcer healing. NF-κB activation was observed in fibroblasts, monocytes/macrophages, and neutrophils. Treatment of gastric fibroblasts, isolated from the ulcer base, with interleukin-1β activated NF-κB and the subsequently induced cyclooxygenase-2 and cytokine-induced neutrophil chemoattractant-1 (CINC-1) mRNA expression. Inhibition of activated NF-κB action resulted in suppression of both their mRNA expression and increases in PGE2 and CINC-1 levels induced by interleukin-1β. Persistent prevention of NF-κB activation caused an impairment of ulcer healing in rats. Gene expression of interleukin-1β, CINC-1, cyclooxygenase-2, and inducible nitric oxide synthase in ulcerated tissue had been inhibited before the delay in ulcer healing became manifest. The increased levels of cyclooxygenase-2 protein and PGE2 production were also reduced. These results demonstrate that NF-κB, activated in ulcerated tissue, might upregulate the expression of healing-promoting factors responsible for gastric ulcer healing in rats.


2003 ◽  
Vol 353 (2) ◽  
pp. 79-82 ◽  
Author(s):  
Francesca Mancini ◽  
Carla Landolfi ◽  
Marta Muzio ◽  
Luciano Aquilini ◽  
Lucia Soldo ◽  
...  

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