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@ARTICLE{DellAlbani:120569,
author = {P. Dell'Albani and B. Di Marco$^*$ and S. Grasso and C.
Rocco and M. C. Foti},
title = {{Q}uercetin derivatives as potent inducers of selective
cytotoxicity in glioma cells.},
journal = {European journal of pharmaceutical sciences},
volume = {101},
issn = {0928-0987},
address = {New York, NY [u.a.]},
publisher = {Elsevier},
reportid = {DKFZ-2017-00998},
pages = {56 - 65},
year = {2017},
abstract = {Quercetin (Q) is a flavonoid widely distributed in the
plant kingdom and well-known for its ability to exert
antioxidant, prooxidant and anticarcinogenic activities in
several tumor cells. Furthermore, quercetin plays an
important role both in the regulation of key elements in
cellular signal transduction pathways related to apoptotic
cell death, and in cell cycle progression. Several studies
have reported of toxic effects of Q against glioma cell
lines. In this study, the effects of Q and of some
Q-derivatives (acyl esters and bromo-derivatives) on U373-MG
and 9L glioma cell lines survival are analyzed. The 24-hour
treatment of glioma cells with several concentrations of Q
(25, 50 and 100μM) did not cause any cytotoxic effects,
while the administration of Q-derivatives, such as acylated
and brominated quercetin, caused a sharp increase in cell
death. Among all tested derivatives, 3-O-decanoylquercetin
10 manifested the strongest cytotoxic effect at a
concentration as low as 25μM both in U373-MG (ca. $40\%$
viability after 24h) and in 9L cells (ca. $20\%$ viability
after 24h). The cytotoxic effects of the Q-derivatives 3 and
10-13 were proven to be satisfactorily selective for glioma
cells. When Q-derivatives were in fact administered to mouse
primary astroglial or human fibroblast cell cultures, a
higher cell survival rate $(~90-70\%$ and $55-45\%,$
respectively) was observed relative to that detected in
glioma cells. These results prove that selective
esterification and bromination of Q increase to a great
extent the toxicity of this polyphenol against glioma cells,
thereby providing a possible new tool for cyto-specific
glioma therapy.},
cin = {A231},
ddc = {610},
cid = {I:(DE-He78)A231-20160331},
pnm = {311 - Signalling pathways, cell and tumor biology
(POF3-311)},
pid = {G:(DE-HGF)POF3-311},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:28153636},
doi = {10.1016/j.ejps.2017.01.036},
url = {https://inrepo02.dkfz.de/record/120569},
}