Modulation of pro- and anti-apoptotic factors in human melanoma cells exposed to histone deacetylase inhibitors

Abstract

In the latter, since activation of caspase 8 was documented, a receptor-mediated apoptosis was suggested. Taken together, our results suggest that HDAC inhibitors may represent a promising therapeutic strategy to treat melanoma.

Apoptosis induced by histone deacetylase inhibitors in leukemic cells is mediated by Bim and Noxa

“…The mechanism whereby HDACi increase Noxa expression is beyond the scope of the current manuscript, although some of the increased expression is clearly due to an upregulation of mRNA for Noxa (Figure 3d). Although some studies in melanoma cells have noted that HDACi do not induce Noxa expression, 41 the increase in Noxa observed in hemopoietic cells in the present study may not be entirely surprising as Noxa shows an elevated expression in the hemopoietic system particularly in B cells. 42 In addition, it has been recently shown that CLL cells express high levels of Noxa mRNA.…”

Synthesis of 1,2-benzisoxazole tethered 1,2,3-triazoles that exhibit anticancer activity in acute myeloid leukemia cell lines by inhibiting histone deacetylases, and inducing p21 and tubulin acetylation

“…This is a target family known to be involved in apoptosis modulation, 45 which we hence decided to follow up first in a structure-based manner, in order to gain more support for our hypothesis that PTB targets HDACs on the interaction level, and subsequently also to confirm the predictions experimentally.…”

Valproic acid induces extracellular signal-regulated kinase 1/2 activation and inhibits apoptosis in endothelial cells

“…16 VPA induces apoptosis in a limited number of cell types while being nontoxic or even cytoprotective in other cells. 5,[17][18][19] In different cells, VPA was shown to stimulate the phosphorylation/activation of the extracellular signal-regulated kinases 1/2 (ERK 1/2, mitogen-activated protein kinase (MAPK)), 15,20 which play an integral role in cellular survival signalling. 21 Since VPA was shown to inhibit endothelial cell proliferation and tube formation but not to exert cytotoxicity in these cells, 11 we determined the influence of VPA on ERK 1/2 activation and on stress-induced cell death in response to serum starvation.…”