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@ARTICLE{Kolbinger:136746,
author = {F. Kolbinger$^*$ and E. Koeneke$^*$ and J. Ridinger$^*$ and
T. Heimburg and M. Müller$^*$ and T. Bayer and W. Sippl and
M. Jung and N. Gunkel$^*$ and A. Miller$^*$ and F.
Westermann$^*$ and O. Witt$^*$ and I. Oehme$^*$},
title = {{T}he {HDAC}6/8/10 inhibitor {TH}34 induces {DNA}
damage-mediated cell death in human high-grade neuroblastoma
cell lines.},
journal = {Archives of toxicology},
volume = {92},
number = {8},
issn = {1432-0738},
address = {Berlin},
publisher = {Springer},
reportid = {DKFZ-2018-01184},
pages = {2649 - 2664},
year = {2018},
abstract = {High histone deacetylase (HDAC) 8 and HDAC10 expression
levels have been identified as predictors of exceptionally
poor outcomes in neuroblastoma, the most common extracranial
solid tumor in childhood. HDAC8 inhibition synergizes with
retinoic acid treatment to induce neuroblast maturation in
vitro and to inhibit neuroblastoma xenograft growth in vivo.
HDAC10 inhibition increases intracellular accumulation of
chemotherapeutics through interference with lysosomal
homeostasis, ultimately leading to cell death in cultured
neuroblastoma cells. So far, no HDAC inhibitor covering
HDAC8 and HDAC10 at micromolar concentrations without
inhibiting HDACs 1, 2 and 3 has been described. Here, we
introduce TH34 (3-(N-benzylamino)-4-methylbenzhydroxamic
acid), a novel HDAC6/8/10 inhibitor for neuroblastoma
therapy. TH34 is well-tolerated by non-transformed human
skin fibroblasts at concentrations up to 25 µM and
modestly impairs colony growth in medulloblastoma cell
lines, but specifically induces caspase-dependent programmed
cell death in a concentration-dependent manner in several
human neuroblastoma cell lines. In addition to the induction
of DNA double-strand breaks, HDAC6/8/10 inhibition also
leads to mitotic aberrations and cell-cycle arrest.
Neuroblastoma cells display elevated levels of neuronal
differentiation markers, mirrored by formation of
neurite-like outgrowths under maintained TH34 treatment.
Eventually, after long-term treatment, all neuroblastoma
cells undergo cell death. The combination of TH34 with
plasma-achievable concentrations of retinoic acid, a drug
applied in neuroblastoma therapy, synergistically inhibits
colony growth (combination index (CI) < 0.1 for 10 µM of
each). In summary, our study supports using selective HDAC
inhibitors as targeted antineoplastic agents and underlines
the therapeutic potential of selective HDAC6/8/10 inhibition
in high-grade neuroblastoma.},
cin = {G340 / L101 / G404 / B087},
ddc = {610},
cid = {I:(DE-He78)G340-20160331 / I:(DE-He78)L101-20160331 /
I:(DE-He78)G404-20160331 / I:(DE-He78)B087-20160331},
pnm = {317 - Translational cancer research (POF3-317)},
pid = {G:(DE-HGF)POF3-317},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:29947893},
pmc = {pmc:PMC6063332},
doi = {10.1007/s00204-018-2234-8},
url = {https://inrepo02.dkfz.de/record/136746},
}