The binding between anticancer drugs and double-stranded DNA (dsDNA) is a key issue to understand their mechanism of action, and many chemical methods have been explored on this task. Molecular docking techniques successfully predict the affinity of small molecules into the DNA binding sites. In turn, various DNA-targeted drugs are electroactive; in this regard, their electrochemical behavior may change according to the nature and strength of interaction with DNA. A carbon paste electrode (CPE) modified with calf thymus ds-DNA (CPDE) and computational methods were used to evaluate the drug-DNA intercalation of doxorubicin (DOX), daunorubicin (DAU), idarubicin (IDA), dacarbazine (DAR), mitoxantrone (MIT), and methotrexate (MTX), aiming to evaluate eventual correlations. CPE and CPDE were immersed in pH 7 0.1 mM solutions of each drug with different incubation times. As expected, the CPDE response for all DNA-targeted drugs was higher than that of CPE, evidencing the drug-DNA interaction. A peak current increase of up to 10-fold was observed; the lowest increase was seen for MTX, and the highest increase for MIT. Although this increase in the sensitivity is certainly tied to preconcentration effects of DNA, the data did not agree entirely with docking studies, evidencing the participation of other factors, such as viscosity, interfacial electrostatic interactions, and coefficient of diffusion.
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http://dx.doi.org/10.3390/molecules26247623 | DOI Listing |
Cardiovasc Res
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Department of Cardiology, Angiology, and Intensive Care Medicine, Deutsches Herzzentrum der Charité, Berlin, Hindenburgdamm 30, 12203 Berlin, Germany.
Nucleic acid-based therapies are being rapidly developed for prevention and management of cardiovascular diseases (CVD). Remarkable advancements have been achieved in the delivery, safety, and effectiveness of these therapeutics in the past decade. These therapies can also modulate therapeutic targets that cannot be sufficiently addressed using traditional drugs or antibodies.
View Article and Find Full Text PDFPLoS One
May 2024
Therapeutic Chemistry Department, National Research Center, Al Bhoouth Street, Cairo, Egypt.
CRISPR/Cas9 is a recently discovered genomic editing technique that altered scientist's sight in studying genes function. Cas9 is controlled via guide (g) RNAs, which match the DNA targeted in cleavage to modify the respective gene. The development in prostate cancer (PC) modeling directed not only to novel resources for recognizing the signaling pathways overriding prostate cell carcinoma, but it has also created a vast reservoir for complementary tools to examine therapies counteracting this type of cancer.
View Article and Find Full Text PDFADMET DMPK
March 2024
Department of Analytical Chemistry, Faculty of Pharmacy, Izmir Katip Celebi University, Izmir, Türkiye.
Background And Purpose: In this study, we present an electrochemical sensor for the detection of oxypeucedanin (Oxyp) and prantschimgin (Pra), two natural furanocoumarin derivatives. The determination of the effects of these molecules on DNA is important to be potential drug candidates. Our research focused on exploring the electrochemical behaviour of these compounds and their interaction with DNA.
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July 2024
Developmental Therapeutics Branch and Pediatric Oncology Branch, Center for Cancer Research, NCI, NIH, Bethesda, Maryland.
Ataxia telangiectasia and Rad3-related (ATR) checkpoint kinase inhibitors are in clinical trials. Here we explored the molecular pharmacology and therapeutic combination strategies of the oral ATR inhibitor M1774 (Tuvusertib) with DNA-damaging agents (DDA). As single agent, M1774 suppressed cancer cell viability at nanomolar concentrations, showing greater activity than ceralasertib and berzosertib, but less potency than gartisertib and elimusertib in the small cell lung cancer H146, H82, and DMS114 cell lines.
View Article and Find Full Text PDFCancer Res
April 2024
Centre de Recherches en Cancérologie de Toulouse, CRCT, Université de Toulouse, Inserm, CNRS, Toulouse, France.
Unlabelled: Cytidine deaminase (CDA) functions in the pyrimidine salvage pathway for DNA and RNA syntheses and has been shown to protect cancer cells from deoxycytidine-based chemotherapies. In this study, we observed that CDA was overexpressed in pancreatic adenocarcinoma from patients at baseline and was essential for experimental tumor growth. Mechanistic investigations revealed that CDA localized to replication forks where it increased replication speed, improved replication fork restart efficiency, reduced endogenous replication stress, minimized DNA breaks, and regulated genetic stability during DNA replication.
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