Differential effects of hydroxamate histone deacetylase inhibitors on cellular functionality and gap junctions in primary cultures of mitogen-stimulated hepatocytes

2008 ◽  
Vol 178 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Tom Henkens ◽  
Mathieu Vinken ◽  
Aneta Lukaszuk ◽  
Dirk Tourwé ◽  
Tamara Vanhaecke ◽  
...  
Keyword(s):  
Gap Junctions ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
Primary Cultures ◽  
Differential Effects

Differential Effects of Histone Deacetylase Inhibitors in Tumor and Normal Cells—What Is the Toxicological Relevance?

2005 ◽  
Vol 35 (4) ◽  
pp. 363-378 ◽  
Author(s):  
Peggy Papeleu ◽  
Tamara Vanhaecke ◽  
Greetje Elaut ◽  
Mathieu Vinken ◽  
Tom Henkens ◽  
...  
Keyword(s):  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
Normal Cells ◽  
Differential Effects

Differential Effects of Histone Deacetylase Inhibitors on Interleukin-18 Gene Expression in Myeloid Cells

2002 ◽  
Vol 292 (4) ◽  
pp. 937-943 ◽  
Author(s):  
Noriko Koyama ◽  
Steffen Koschmieder ◽  
Sandhya Tyagi ◽  
Heike Nürnberger ◽  
Sandra Wagner ◽  
...  
Keyword(s):  
Gene Expression ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
Myeloid Cells ◽  
Interleukin 18 ◽  
Differential Effects

scholarly journals Synergistic antitumor activity of histone deacetylase inhibitors and anti-ErbB3 antibody in NSCLC primary cultures via modulation of ErbB receptors expression

Oncotarget ◽  
2016 ◽  
Vol 7 (15) ◽  
pp. 19559-19574 ◽  
Author(s):  
Chiara Ciardiello ◽  
Maria Serena Roca ◽  
Alessia Noto ◽  
Francesca Bruzzese ◽  
Tania Moccia ◽  
...  
Keyword(s):  
Antitumor Activity ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
Primary Cultures ◽  
Erbb Receptors ◽  
Synergistic Antitumor Activity

Differential effects of histone deacetylase inhibitors on hypertrophic signaling pathways

2004 ◽  
Vol 10 (4) ◽  
pp. S60
Author(s):  
Hansjorg Rindt ◽  
Matthew Dreitz ◽  
Lisa Hollingsworth ◽  
David Hood ◽  
Erik Bush ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
Differential Effects ◽  
Hypertrophic Signaling

scholarly journals Differential effects of histone deacetylase inhibitors on transcription factor dynamics and activity at the same response element

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Martina Tesikova ◽  
Xavier Dezitter ◽  
Tove I. Klokk ◽  
Zeynep Kirli ◽  
Gordon L. Hager ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
Response Element ◽  
Differential Effects

scholarly journals MiR-129-5p is required for histone deacetylase inhibitor-induced cell death in thyroid cancer cells

2011 ◽  
Vol 18 (6) ◽  
pp. 711-719 ◽  
Author(s):  
Patrick Brest ◽  
Sandra Lassalle ◽  
Veronique Hofman ◽  
Olivier Bordone ◽  
Virginie Gavric Tanga ◽  
...  
Keyword(s):  
Cell Death ◽  
Thyroid Cancer ◽  
Antitumor Activity ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
Trichostatin A ◽  
Primary Cultures ◽  
Cancer Drugs ◽  
Deacetylase Inhibitor ◽  
Thyroid Cancer Cells

The molecular mechanism responsible for the antitumor activity of histone deacetylase inhibitors (HDACi) remains elusive. As HDACi have been described to alter miRNA expression, the aim of this study was to characterize HDACi-induced miRNAs and to determine their functional importance in the induction of cell death alone or in combination with other cancer drugs. Two HDACi, trichostatin A and vorinostat, induced miR-129-5p overexpression, histone acetylation and cell death in BCPAP, TPC-1, 8505C, and CAL62 cell lines and in primary cultures of papillary thyroid cancer (PTC) cells. In addition, miR-129-5p alone was sufficient to induce cell death and knockdown experiments showed that expression of this miRNA was required for HDACi-induced cell death. Moreover, miR-129-5p accentuated the anti-proliferative effects of other cancer drugs such as etoposide or human α-lactalbumin made lethal for tumor cells (HAMLET). Taken together, our data show that miR-129-5p is involved in the antitumor activity of HDACi and highlight a miRNA-driven cell death mechanism.

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