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Special Issue "Biology and Development of Therapeutic Drugs Targeting DNA"

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1. Center for Bioinformatics and Molecular Medicine, Department of Molecular and Genomic Biomedicine, Nagasaki University Graduate School of Biomedical Sciences, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan
2. Central Radioisotope Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan
Interests: radiation oncology; biology in anti-cancer treatment; poly ADP-ribosylation
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Dr. Tadayoshi Bessho

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The Eppley Institute for Research in Cancer and Allied Diseases, Fred & Pamela Buffett Cancer Center, University of Nebraska Medical Center, Omaha, NE 68198-6805, USA
Interests: DNA repair/DNA damage response; nucleotide excision repair (NER); double strand break (DSB) repair; DNA interstrand cross-link (ICL) repair; DNA protein cross-link (DPC) repair; base excision repair (BER)
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

DNA-targeting drugs that directly interact with DNA, such as alkylating, crosslinking, and DNA intercalating agents have been used in cancer chemotherapies for decades with some success. Recently, drugs that selectively target DNA repair factors have been developed, with some of these drugs currently under clinical trial. DNA repair inhibitors with a selective target, such as inhibitors of poly(ADP-ribose) polymerase, indirectly introduce lethal DNA damage to cancer cells. Inhibitors of epigenetic and chromatin regulation also indirectly target DNA, causing cancer cell death. DNA targeting drugs that induce lethal DNA damage directly or indirectly will become a critical component of effective cancer chemotherapies in the future. Thus, this Special Issue will focus on the use of DNA targeting drugs, namely those that target DNA repair and epigenetic and chromatin regulation, for various diseases, including cancers. Authors are invited to submit original research articles and reviews on various types of molecular and biological aspects of DNA targeting drugs for inclusion in this Special Issue.

Dr. Mitsuko Masutani
Dr. Tadayoshi Bessho
Guest Editors

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Keywords

DNA targeting drugs
DNA repair/DNA damage response
molecular targeted therapy

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Research

17 pages, 2109 KiB

Open AccessArticle

Characterization of Systemic and Culprit-Coronary Artery miR-483-5p Expression in Chronic CAD and Acute Myocardial Infarction Male Patients

and

Int. J. Mol. Sci. 2023, 24(10), 8551; https://doi.org/10.3390/ijms24108551 - 10 May 2023

Viewed by 1141

Abstract

Coronary artery disease (CAD) is the leading cause of mortality worldwide. In chronic and myocardial infarction (MI) states, aberrant levels of circulating microRNAs compromise gene expression and pathophysiology. We aimed to compare microRNA expression in chronic-CAD and acute-MI male patients in peripheral blood vasculature versus coronary arteries proximal to a culprit area. Blood from chronic-CAD, acute-MI with/out ST segment elevation (STEMI/NSTEMI, respectively), and control patients lacking previous CAD or having patent coronary arteries was collected during coronary catheterization from peripheral arteries and from proximal culprit coronary arteries aimed for the interventions. Random coronary arterial blood was collected from controls; RNA extraction, miRNA library preparation and Next Generation Sequencing followed. High concentrations of microRNA-483-5p (miR-483-5p) were noted as ‘coronary arterial gradient’ in culprit acute-MI versus chronic-CAD (p = 0.035) which were similar to controls versus chronic-CAD (p < 0.001). Meanwhile, peripheral miR-483-5p was downregulated in acute-MI and chronic-CAD, compared with controls (1.1 ± 2.2 vs. 2.6 ± 3.3, respectively, p < 0.005). A receiver operating characteristic curve analysis for miR483-5p association with chronic CAD demonstrated an area under the curve of 0.722 (p < 0.001) with 79% sensitivity and 70% specificity. Using in silico gene analysis, we detected miR-483-5p cardiac gene targets, responsible for inflammation (PLA2G5), oxidative stress (NUDT8, GRK2), apoptosis (DNAAF10), fibrosis (IQSEC2, ZMYM6, MYOM2), angiogenesis (HGSNAT, TIMP2) and wound healing (ADAMTS2). High miR-483-5p ‘coronary arterial gradient’ in acute-MI, unnoticed in chronic-CAD, suggests important local mechanisms for miR483-5p in CAD in response to local myocardial ischemia. MiR-483-5p may have an important role as a gene modulator for pathologic and tissue repair states, is a suggestive biomarker, and is a potential therapeutic target for acute and chronic cardiovascular disease. Full article

(This article belongs to the Special Issue Biology and Development of Therapeutic Drugs Targeting DNA)

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21 pages, 3139 KiB

Open AccessArticle

Spectroscopic Characterization and Biological Activity of Hesperetin Schiff Bases and Their Cu(II) Complexes

Magdalena Rowińska-Żyrek

Justyna Czerwińska

Waldemar Maniukiewicz

and

Elżbieta Łodyga-Chruścińska

Int. J. Mol. Sci. 2023, 24(1), 761; https://doi.org/10.3390/ijms24010761 - 01 Jan 2023

Cited by 3 | Viewed by 1452

Abstract

The three Schiff base ligands, derivatives of hesperetin, HHSB (N-[2,3-dihydro-5,7-dihydroxy-2-(3-hydroxy-4-methoxyphenyl)chromen-4-ylidene]isonicotinohydrazide), HIN (N-[2,3-dihydro-5,7-dihydroxy-2-(3-hydroxy-4-methoxyphenyl)chromen-4-ylidene]benzhydrazide) and HTSC (N-[2,3-dihydro-5,7-dihydroxy-2-(3-hydroxy-4-methoxyphenyl)chromen-4-ylidene]thiosemicarbazide) and their copper complexes, CuHHSB, CuHIN, and CuHTSC were designed, synthesized and analyzed in terms of their spectral characterization and the genotoxic activity. Their structures were established using several methods: elemental analysis, FT-IR, UV-Vis, EPR, and ESI-MS. Spectral data showed that in the acetate complexes the tested Schiff bases act as neutral tridentate ligand coordinating to the copper ion through two oxygen (or oxygen and sulphur) donor atoms and a nitrogen donor atom. EPR measurements indicate that in solution the complexes keep their structures with the ligands remaining bound to copper(II) in a tridentate fashion with (O^–, N, O_ket) or (O^–, N, S) donor set. The genotoxic activity of the compounds was tested against model tumour (HeLa and Caco-2) and normal (LLC-PK1) cell lines. In HeLa cells the genotoxicity for all tested compounds was noticed, for HHSB and CuHHSB was the highest, for HTSC and CuHTSC–the lowest. Generally, Cu complexes displayed lower genotoxicity to HeLa cells than ligands. In the case of Caco-2 cell line HHSB and HTSC induced the strongest breaks to DNA. On the other side, CuHHSB and CuHTSC induced the highest DNA damage against LLC-PK1. Full article

(This article belongs to the Special Issue Biology and Development of Therapeutic Drugs Targeting DNA)

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