ChemInform Abstract: Novel Isatin-Based Hydroxamic Acids as Histone Deacetylase Inhibitors and Antitumor Agents.

ChemInform ◽  
2014 ◽  
Vol 45 (20) ◽  
pp. no-no
Author(s):  
Nguyen-Hai Nam ◽  
et al. et al.
2013 ◽  
Vol 9 (8) ◽  
pp. 1051-1057 ◽  
Author(s):  
Truong Tung ◽  
Dao Kim Oanh ◽  
Phan Phuong Dung ◽  
Van My Hue ◽  
Sang Park ◽  
...  

2013 ◽  
Vol 70 ◽  
pp. 477-486 ◽  
Author(s):  
Nguyen-Hai Nam ◽  
Tran Lan Huong ◽  
Do Thi Mai Dung ◽  
Phan Thi Phuong Dung ◽  
Dao Thi Kim Oanh ◽  
...  

2011 ◽  
Vol 21 (24) ◽  
pp. 7509-7512 ◽  
Author(s):  
Dao Thi Kim Oanh ◽  
Hoang Van Hai ◽  
Sang Ho Park ◽  
Hyun-Jung Kim ◽  
Byung-Woo Han ◽  
...  

2020 ◽  
Vol 101 ◽  
pp. 103988
Author(s):  
Duong Tien Anh ◽  
Pham-The Hai ◽  
Le-Thi-Thu Huong ◽  
Eun Jae Park ◽  
Hye Won Jun ◽  
...  

2017 ◽  
Vol 71 (9) ◽  
pp. 1759-1769 ◽  
Author(s):  
Tran Thi Lan Huong ◽  
Le Van Cuong ◽  
Pham Thu Huong ◽  
Tran Phuong Thao ◽  
Le-Thi-Thu Huong ◽  
...  

2005 ◽  
Vol 25 (5) ◽  
pp. 1608-1619 ◽  
Author(s):  
Hong Duan ◽  
Caroline A. Heckman ◽  
Linda M. Boxer

ABSTRACT Histone deacetylase (HDAC) inhibitors are promising antitumor agents, but they have not been extensively explored in B-cell lymphomas. Many of these lymphomas have the t(14;18) translocation, which results in increased bcl-2 expression and resistance to apoptosis. In this study, we examined the effects of two structurally different HDAC inhibitors, trichostatin A (TSA) and sodium butyrate (NaB), on the cell cycle, apoptosis, and bcl-2 expression in t(14;18) lymphoma cells. We found that in addition to potent cell cycle arrest, TSA and NaB also dramatically induced apoptosis and down-regulated bcl-2 expression, and overexpression of bcl-2 inhibited TSA-induced apoptosis. The repression of bcl-2 by TSA occurred at the transcriptional level. Western blot analysis and quantitative chromatin immunoprecipitation (ChIP) assay showed that even though HDAC inhibitors increased overall acetylation of histones, localized histone H3 deacetylation occurred at both bcl-2 promoters. TSA treatment increased the acetylation of the transcription factors Sp1 and C/EBPα and decreased their binding as well as the binding of CBP and HDAC2 to the bcl-2 promoters. Mutation of Sp1 and C/EBPα binding sites reduced the TSA-induced repression of bcl-2 promoter activity. This study provides a mechanistic rationale for the use of HDAC inhibitors in the treatment of human t(14;18) lymphomas.


2015 ◽  
Vol 25 (7) ◽  
pp. 1603-1606 ◽  
Author(s):  
Elena Marastoni ◽  
Sandra Bartoli ◽  
Marco Berettoni ◽  
Amalia Cipollone ◽  
Alessandro Ettorre ◽  
...  

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