Comparative thermal and thermodynamic study of DNA chemically modified with antitumor drug cisplatin and its inactive analog transplatin

Lando, Dmitri Y.; Chang, C.; Fridman, Alexander S.; Grigoryan, Inessa E.; Galyuk, Elena N.; Hsueh, Ya-Wei; Hu, Chin Kun

doi:10.1016/j.jinorgbio.2014.04.010

Cited by 12 publications

(5 citation statements)

References 61 publications

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“…Cisplatin is known to cause inter- and intra-strand DNA crosslinks, which perturbs DNA replication and transcription, thereby inducing a replication stress and DDR, which may eventually result in cell cycle arrest and cell apoptosis(Fig. 1) (Dasari and Tchounwou 2014; Fujikawa et al 2014; Kruger et al 2015; Lando et al 2014; Roos and Kaina 2013; Wang and Lippard 2005). This review will elucidate DDR, its regulatory mechanisms, and pathological role in cisplatin-AKI.…”

Section: Introductionmentioning

confidence: 99%

DNA damage response in cisplatin-induced nephrotoxicity

et al. 2015

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Cisplatin and its derivatives are widely used chemotherapeutic drugs for cancer treatment. However, they have debilitating side-effects in normal tissues and induce ototoxicity, neurotoxicity, and nephrotoxicity. In kidneys, cisplatin preferentially accumulates in renal tubular cells causing tubular cell injury and death, resulting in acute kidney injury (AKI). Recent studies have suggested that DNA damage and the associated DNA damage response (DDR) is an important pathogenic mechanism of AKI following cisplatin treatment. Activation of DDR may lead to cell cycle arrest and DNA repair for cell survival or, in the presence of severe injury, kidney cell death. Modulation of DDR may provide novel renoprotective strategies for cancer patients undergoing cisplatin chemotherapy.

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Section: Introductionmentioning

confidence: 99%

DNA damage response in cisplatin-induced nephrotoxicity

et al. 2015

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“…The DNA melting temperature T intR and temperature melting range Δ T σR were determined using the following definitions:

T_{int R} = \int_{T s}^{T e} T \cdot ϑ' false(T false) \cdot d T

Δ T_{σ R} = {false(2 π false)}^{1 / 2} {[true \int_{T s}^{T e} {false(T - T_{intR} false)}^{2} \cdot ϑ' (T) \cdot d T]}^{1 / 2}

where T s and T e are the temperatures of the start and end of the helix‐coil transition, respectively. The same parameters ( T intC and Δ T σC ) were also calculated for the differential calorimetric melting curve (cDMC) ϑ cal ′( T ) by the replacement of ϑ′( T ) with ϑ cal ′( T ) and T intR with T intC in ),.…”

Section: Methodsmentioning

confidence: 99%

Estimation of the diversity between DNA calorimetric profiles, differential melting curves and corresponding melting temperatures

et al. 2016

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The Poland-Fixman-Freire formalism was adapted for modeling of calorimetric DNA melting profiles, and applied to plasmid pBR 322 and long random sequences. We studied the influence of the difference (HGC -HAT ) between the helix-coil transition enthalpies of AT and GC base pairs on the calorimetric melting profile and on normalized calorimetric melting profile. A strong alteration of DNA calorimetrical profile with HGC -HAT was demonstrated. In contrast, there is a relatively slight change in the normalized profiles and in corresponding ordinary (optical) normalized differential melting curves (DMCs). For fixed HGC -HAT , the average relative deviation (S) between DMC and normalized calorimetric profile, and the difference between their melting temperatures (Tcal -Tm ) are weakly dependent on peculiarities of the multipeak fine structure of DMCs. At the same time, both the deviation S and difference (Tcal -Tm ) enlarge with the temperature melting range of the helix-coil transition. It is shown that the local deviation between DMC and normalized calorimetric profile increases in regions of narrow peaks distant from the melting temperature.

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“…The temperature at which 50 % of the double-stranded DNA remains in the doublestranded state is considered the DNA melting temperature (Tm) 61 . The melting temperature of DNA (Tm) directly depends on the stability of its double helix.…”

Section: Binding To Dnamentioning

confidence: 99%

Atranorin is a novel potential candidate drug for treating myelodysplastic syndrome

Semenov,

Prokopiev,

Petukhova

et al. 2024

Preprint

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This work is devoted to the study of biocompatibility, cyto- and genotoxicity, mechanism of action and prospects for the use of atranorin, which is an AKT kinase inhibitor, for the treatment of myelodysplastic syndrome. Atranorin was isolated by preparative flash chromatography; identification was carried out by UV, IR, and NMR spectroscopy, mass spectrometry, and elemental analysis. Biocompatibility studies included studies of haemocompatibility, genotoxicity, antioxidant activity, cytotoxicity against ECV340 and HEK293 cell lines. Computer modelling of the interaction of atranorin with AKT kinase was carried out using docking followed by molecular dynamics of the resulting complexes; the ADMET properties of atranorin were also calculated. Flow cytometry included analysis of the expression level of PD-L1 and TIM-3 in the presence of atranorin on THP-1, Mono-Mac-1 and KG-1 cell lines, as well as human bone marrow cells.

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Comparative thermal and thermodynamic study of DNA chemically modified with antitumor drug cisplatin and its inactive analog transplatin

Cited by 12 publications

References 61 publications

DNA damage response in cisplatin-induced nephrotoxicity

DNA damage response in cisplatin-induced nephrotoxicity

Estimation of the diversity between DNA calorimetric profiles, differential melting curves and corresponding melting temperatures

Atranorin is a novel potential candidate drug for treating myelodysplastic syndrome

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