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Molecules
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Research and Development of DNA Repair Inhibitors
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Research and Development of DNA Repair Inhibitors

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Medicinal Chemistry".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 7419

Special Issue Editors

Prof. Dr. Benoît Chénais

E-Mail Website
Guest Editor
BiOSSE (Biology of Organisms: Stress, Health, Environment), UFR Sciences et Techniques, Le Mans Université, CEDEX 9, F-72085 Le Mans, France
Interests: cancer cell biology; DNA repair; transposable elements; bioactive molecules; gene expression; stress response; microalgae
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Fabrice Fleury

E-Mail Website
Guest Editor
UMR 6286 CNRS Unité Fonctionnalité et Ingénierie des Protéines, Université de Nantes, F-44000 Nantes, France
Interests: cancer cell biology; DNA repair; Rad51 inhibitors; post-translational modification

Special Issue Information

Dear Colleagues,

All living organisms are constantly confronted to numerous DNA lesions, which may be induced by both exogenous agents (chemical agents, ionizing radiation) and endogenous factors such as reactive oxygen species (ROS) derived from normal cellular metabolism. Therefore, to maintain DNA integrity, cells possess a surveillance network for sensing and repairing DNA damage. Proteins involved in the DNA repair pathway are essential for the genomic stability preventing genome mutations but can also promote drug resistance when their activities are deregulated. Understanding the regulation and functions of these mechanisms are important in human cells but also in other organisms such as in bacteria or in parasites.

Since these DNA repair proteins have been conserved during biological evolution, they represent potential targets to support classical antiproliferative cancer therapies and to overcome certain human diseases such as bacterial infections, fungal proliferation, parasitosis, viral infections, etc.

Thus, the development of effective inhibitors of the DNA repair machinery appears to be a pharmacological challenge addressing a wide range of pathophysiological situations that need to be controlled.

Whether derived from natural substances or from synthetic chemistry, there are few inhibitors of DNA repair and the characterization of new inhibitors is necessary.

The aim of this special issue is to present current data on already known inhibitors of DNA repair and to highlight new candidates from nature or chemistry.

Prof. Dr. Benoît Chénais
Prof. Dr. Fabrice Fleury
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Molecules is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • DNA repair 
  • Homologous recombination 
  • Rad51 
  • BRCA 
  • Non-Homologous End Joining 
  • Cancer 
  • Bacterial infection 
  • Viral infection 
  • …/…

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Published Papers (2 papers)

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Research

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11 pages, 1628 KiB  
Article
The Influence of 5′R and 5′S cdA and cdG on the Activity of BsmAI and SspI Restriction Enzymes
by Michał Szewczuk, Karolina Boguszewska, Julia Kaźmierczak-Barańska and Bolesław T. Karwowski
Molecules 2021, 26(12), 3750; https://doi.org/10.3390/molecules26123750 - 19 Jun 2021
Cited by 3 | Viewed by 2341
Abstract
Restriction endonucleases (REs) are intra-bacterial scissors that are considered tools in the fight against foreign genetic material. SspI and BsmAI, examined in this study, cleave dsDNA at their site of recognition or within a short distance of it. Both enzymes are representatives of [...] Read more.
Restriction endonucleases (REs) are intra-bacterial scissors that are considered tools in the fight against foreign genetic material. SspI and BsmAI, examined in this study, cleave dsDNA at their site of recognition or within a short distance of it. Both enzymes are representatives of type II REs, which have played an extremely important role in research on the genetics of organisms and molecular biology. Therefore, the study of agents affecting their activity has become highly important. Ionizing radiation may damage basic cellular mechanisms by inducing lesions in the genome, with 5′,8-cyclo-2′-deoxypurines (cdPus) as a model example. Since cdPus may become components of clustered DNA lesions (CDLs), which are unfavorable for DNA repair pathways, their impact on other cellular mechanisms is worthy of attention. This study investigated the influence of cdPus on the elements of the bacterial restriction–modification system. In this study, it was shown that cdPus present in DNA affect the activity of REs. SspI was blocked by any cdPu lesion present at the enzyme’s recognition site. When lesions were placed near the recognition sequence, the SspI was inhibited up to 46%. Moreover, (5′S)-5′,8-cyclo-2′-deoxyadenosine (ScdA) present in the oligonucleotide sequence lowered BsmAI activity more than (5′R)-5′,8-cyclo-2′-deoxyadenosine (RcdA). Interestingly, in the case of 5′,8-cyclo-2′-deoxyguanosine (cdG), both 5′S and 5′R diastereomers inhibited BsmAI activity (up to 55% more than cdA). The inhibition was weaker when cdG was present at the recognition site rather than the cleavage site. Full article
(This article belongs to the Special Issue Research and Development of DNA Repair Inhibitors)
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Review

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19 pages, 1150 KiB  
Review
Targeting Replication Stress Response Pathways to Enhance Genotoxic Chemo- and Radiotherapy
by Jac A. Nickoloff
Molecules 2022, 27(15), 4736; https://doi.org/10.3390/molecules27154736 - 25 Jul 2022
Cited by 10 | Viewed by 4149
Abstract
Proliferating cells regularly experience replication stress caused by spontaneous DNA damage that results from endogenous reactive oxygen species (ROS), DNA sequences that can assume secondary and tertiary structures, and collisions between opposing transcription and replication machineries. Cancer cells face additional replication stress, including [...] Read more.
Proliferating cells regularly experience replication stress caused by spontaneous DNA damage that results from endogenous reactive oxygen species (ROS), DNA sequences that can assume secondary and tertiary structures, and collisions between opposing transcription and replication machineries. Cancer cells face additional replication stress, including oncogenic stress that results from the dysregulation of fork progression and origin firing, and from DNA damage induced by radiotherapy and most cancer chemotherapeutic agents. Cells respond to such stress by activating a complex network of sensor, signaling and effector pathways that protect genome integrity. These responses include slowing or stopping active replication forks, protecting stalled replication forks from collapse, preventing late origin replication firing, stimulating DNA repair pathways that promote the repair and restart of stalled or collapsed replication forks, and activating dormant origins to rescue adjacent stressed forks. Currently, most cancer patients are treated with genotoxic chemotherapeutics and/or ionizing radiation, and cancer cells can gain resistance to the resulting replication stress by activating pro-survival replication stress pathways. Thus, there has been substantial effort to develop small molecule inhibitors of key replication stress proteins to enhance tumor cell killing by these agents. Replication stress targets include ATR, the master kinase that regulates both normal replication and replication stress responses; the downstream signaling kinase Chk1; nucleases that process stressed replication forks (MUS81, EEPD1, Metnase); the homologous recombination catalyst RAD51; and other factors including ATM, DNA-PKcs, and PARP1. This review provides an overview of replication stress response pathways and discusses recent pre-clinical studies and clinical trials aimed at improving cancer therapy by targeting replication stress response factors. Full article
(This article belongs to the Special Issue Research and Development of DNA Repair Inhibitors)
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