Decreased serum dependence in the growth of NIH3T3 cells from the overexpression of human nuclear receptor-binding SET-domain-containing protein 1 (NSD1) or fission yeast su(var)3-9, enhancer-of-zeste, trithorax 2 (SET2)

2008 ◽  
Vol 26 (2) ◽  
pp. 146-150 ◽  
Author(s):  
Toshiko Yamada-Okabe ◽  
Naomichi Matsumoto
2021 ◽  
Vol 12 (10) ◽  
Author(s):  
Yihui Sun ◽  
Jiaming Xie ◽  
Shang Cai ◽  
Qian Wang ◽  
Zhenyu Feng ◽  
...  

AbstractThe nuclear receptor-binding SET domain 3 (NSD3) catalyzes methylation of histone H3 at lysine 36 (H3K36), and promotes malignant transformation and progression of human cancer. Its expression, potential functions and underlying mechanisms in pancreatic cancer are studied. Bioinformatics studies and results from local human tissues show that NSD3 is upregulated in human pancreatic cancer tissues, which is correlated with poor overall survival. In primary and established pancreatic cancer cells, NSD3 silencing (by shRNAs) or CRISPR/Cas9-induced NSD3 knockout potently inhibited cell proliferation, migration and invasion, while provoking cell cycle arrest and apoptosis. Conversely, ectopic expression of NSD3-T1232A mutation significantly accelerated proliferation, migration, and invasion of pancreatic cancer cells. H3K36 dimethylation, expression of NSD3-dependent genes (Prkaa2, Myc, Irgm1, Adam12, and Notch3), and mTOR activation (S6K1 phosphorylation) were largely inhibited by NSD3 silencing or knockout. In vivo, intratumoral injection of adeno-associated virus (AAV)-packed NSD3 shRNA potently inhibited pancreatic cancer xenograft growth in nude mice. These results suggest that elevated NSD3 could be an important driver for the malignant progression of pancreatic cancer.


2008 ◽  
Vol 22 (S2) ◽  
pp. 202-202
Author(s):  
Hee‐Bum Kang ◽  
Hyo‐Kyoung Choi ◽  
Kyung‐Chul Choi ◽  
Yoo‐Hyun Lee ◽  
Jung‐Yoon Yoo ◽  
...  

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