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@ARTICLE{Calandrini:280472,
author = {Calandrini, Vania and Rossetti, Giulia and Arnesano, Fabio
and Natile, Giovanni and Carloni, Paolo},
title = {{C}omputational metallomics of the anticancer drug
cisplatin},
journal = {Journal of inorganic biochemistry},
volume = {153},
issn = {0162-0134},
address = {New York, NY [u.a.]},
publisher = {Elsevier},
reportid = {FZJ-2016-00246},
pages = {231 - 238},
year = {2015},
abstract = {Cisplatin, cis-diamminedichlorido-platinum(II), is an
important therapeutic tool in the struggle against different
tumors, yet it is plagued with the emergence of resistance
mechanisms after repeated administrations. This hampers
greatly its efficacy. Overcoming resistance problems
requires first and foremost an integrated and systematic
understanding of the structural determinants and molecular
recognition processes involving the drug and its cellular
targets. Here we review a strategy that we have followed for
the last few years, based on the combination of modern tools
from computational chemistry with experimental biophysical
methods. Using hybrid Quantum Mechanics/Molecular Mechanics
(QM/MM) simulations, validated by spectroscopic experiments
(including NMR, and CD), we have worked out for the first
time at atomic level the structural determinants in solution
of platinated cellular substrates. These include the copper
homeostasis proteins Ctr1, Atox1, and ATP7A. All of these
proteins have been suggested to influence the pre-target
resistance mechanisms. Furthermore, coupling hybrid QM/MM
simulations with classical Molecular Dynamics (MD) and free
energy calculations, based on force field parameters refined
by the so-called “Force Matching” procedure, we have
characterized the structural modifications and the free
energy landscape associated with the recognition between
platinated DNA and the protein HMGB1, belonging to the
chromosomal high-mobility group proteins HMGB that inhibit
the repair of platinated DNA. This may alleviate issues
relative to on-target resistance process. The elucidation of
the mechanisms by which tumors are sensitive or refractory
to cisplatin may lead to the discovery of prognostic
biomarkers. The approach reviewed here could be
straightforwardly extended to other metal-based drugs.},
cin = {IAS-5 / INM-9 / JSC},
ddc = {540},
cid = {I:(DE-Juel1)IAS-5-20120330 / I:(DE-Juel1)INM-9-20140121 /
I:(DE-Juel1)JSC-20090406},
pnm = {511 - Computational Science and Mathematical Methods
(POF3-511) / 572 - (Dys-)function and Plasticity (POF3-572)
/ 574 - Theory, modelling and simulation (POF3-574)},
pid = {G:(DE-HGF)POF3-511 / G:(DE-HGF)POF3-572 /
G:(DE-HGF)POF3-574},
typ = {PUB:(DE-HGF)16},
UT = {WOS:000367563200026},
doi = {10.1016/j.jinorgbio.2015.10.001},
url = {https://juser.fz-juelich.de/record/280472},
}