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The Role of DNA Damage and Repair in Cancer
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The Role of DNA Damage and Repair in Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: closed (31 January 2023) | Viewed by 6517

Special Issue Editor

Dr. Miroslav Chovanec

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Guest Editor
Department of Genetics, Cancer Research Institute, Biomedical Research Center, Slovak Academy of Sciences, Dúbravská cesta 9, 845 05 Bratislava, Slovakia
Interests: DNA damage; DNA repair; cancer; biomarker; targeted therapy; treatment personalization
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

For many decades, genome instability has been recognized as a driving force for the development of cancer, and DNA repair systems as crucial factors ensuring the maintenance of genome stability and prevention of cancer. However, these systems also represent cancer treatment obstacles, particularly in the case of using treatment regimens for which the primary pharmacological target is a DNA molecule. Understandably, DNA repair inhibitors, either alone or in combination, are highly promising anticancer tools necessary for achieving higher curability and longer survival rates. Historically, DNA repair inhibitors (natural or small molecules, epigenetic changes by CpG methylation and miRNA, etc.) have most often been used within a synthetic lethality approach, where they target cancer cells defective in specific DNA repair system(s). Therefore, comprehensive information on the DNA repair efficiency of cancer cells has a strong prognostic and predictive value. Genome instability and the mutation burden in these cancer cells may also have such a value and be targeted in treatment. Collectively, DNA damage and DNA repair pathways are promising cancer biomarkers with high potential for use in personalized treatment approaches.

Authors are warmly invited to submit original research and review articles to this Special Issue which address the latest progress and current understanding of the role of DNA damage and repair in cancer.

Topics include, but are not limited to:

  • Role of genome instability in cancer
  • Prognostic value of genome instability
  • Use of DNA repair inhibitors in cancer treatment
  • Role of DNA repair variants in cancer incidence and treatment
  • Synthetic lethality based on the use of DNA repair inhibitors
  • Targeting of DNA repair by miRNA
  • Loss of DNA repair in cancer
  • Drug targeting of genome instability in cancer
  • DNA repair biomarkers
  • Role of genome instability and DNA repair in tumour mutation load

Dr. Miroslav Chovanec
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • apoptosis
  • DNA damage
  • DNA repair
  • DNA damage response
  • cell cycle
  • DNA repair inhibitors
  • personalized treatment
  • cancer biomarker
  • radiotherapy
  • chemotherapy
  • synthetic lethality
  • DNA repair gene variants
  • tumour mutation burden
  • carcinogenesis
  • mutagenesis

Published Papers (3 papers)

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Research

16 pages, 4044 KiB  
Article
Multiple Perspectives Reveal the Role of DNA Damage Repair Genes in the Molecular Classification and Prognosis of Pancreatic Adenocarcinoma
by Yujie Li, Ke Zhang, Linjia Peng, Lianyu Chen, Huifeng Gao and Hao Chen
Int. J. Mol. Sci. 2022, 23(18), 10231; https://doi.org/10.3390/ijms231810231 - 06 Sep 2022
Viewed by 1482
Abstract
Pancreatic adenocarcinoma (PAAD) is a highly heterogeneous and immunosuppressive cancer. This study investigated the diversity of DNA damage repair (DDR) and immune microenvironment in PAAD by transcriptomic and genomic analysis. Patients with PAAD were divided into two DDR-based subtypes with distinct prognosis and [...] Read more.
Pancreatic adenocarcinoma (PAAD) is a highly heterogeneous and immunosuppressive cancer. This study investigated the diversity of DNA damage repair (DDR) and immune microenvironment in PAAD by transcriptomic and genomic analysis. Patients with PAAD were divided into two DDR-based subtypes with distinct prognosis and molecular characteristics. The differential expression genes were mostly enriched in DDR and immune-related pathways. In order to distinguish high- and low-risk groups clinically, a DDR- and immune-based 5-gene prognostic signature (termed DPRS) was established. Patients in the high-risk group had inferior prognosis, a low level of immune checkpoint gene expression and low sensitivity to DDR-associated inhibitors. Furthermore, single-cell sequencing was used to observe the performance of the DDR-based signature in a high dimension, and immunohistochemistry was used to verify the relationship between the genes we identified and the prognosis of patients with PAAD. In conclusion, the DDR heterogeneity of PAAD was demonstrated, and a novel DDR- and immune-based risk-scoring model was constructed, which indicated the feasibility of DPRS in predicting prognosis and drug response in PAAD patients. Full article
(This article belongs to the Special Issue The Role of DNA Damage and Repair in Cancer)
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17 pages, 2704 KiB  
Article
HDAC Inhibitor Sodium Butyrate Attenuates the DNA Repair in Transformed but Not in Normal Fibroblasts
by Olga O. Gnedina, Alisa V. Morshneva, Elena V. Skvortsova and Maria V. Igotti
Int. J. Mol. Sci. 2022, 23(7), 3517; https://doi.org/10.3390/ijms23073517 - 23 Mar 2022
Cited by 3 | Viewed by 2408
Abstract
Many cancer therapy strategies cause DNA damage leading to the death of tumor cells. The DNA damage response (DDR) modulators are considered as promising candidates for use in combination therapy to enhance the efficacy of DNA-damage-mediated cancer treatment. The inhibitors of histone deacetylases [...] Read more.
Many cancer therapy strategies cause DNA damage leading to the death of tumor cells. The DNA damage response (DDR) modulators are considered as promising candidates for use in combination therapy to enhance the efficacy of DNA-damage-mediated cancer treatment. The inhibitors of histone deacetylases (HDACis) exhibit selective antiproliferative effects against transformed and tumor cells and could enhance tumor cell sensitivity to genotoxic agents, which is partly attributed to their ability to interfere with DDR. Using the comet assay and host-cell reactivation of transcription, as well as γH2AX staining, we have shown that sodium butyrate inhibited DNA double-strand break (DSB) repair of both endo- and exogenous DNA in transformed but not in normal cells. According to our data, the dysregulation of the key repair proteins, especially the phosphorylated Mre11 pool decrease, is the cause of DNA repair impairment in transformed cells. The inability of HDACis to obstruct DSB repair in normal cells shown in this work demonstrates the advantages of HDACis in combination therapy with genotoxic agents to selectively enhance their cytotoxic activity in cancer cells. Full article
(This article belongs to the Special Issue The Role of DNA Damage and Repair in Cancer)
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14 pages, 3604 KiB  
Article
Oncolytic Bovine Herpesvirus 1 Inhibits Human Lung Adenocarcinoma A549 Cell Proliferation and Tumor Growth by Inducing DNA Damage
by Wencai Qiu, Xiuyan Ding, Shitao Li, Yongming He and Liqian Zhu
Int. J. Mol. Sci. 2021, 22(16), 8582; https://doi.org/10.3390/ijms22168582 - 10 Aug 2021
Cited by 10 | Viewed by 1846
Abstract
Bovine herpesvirus 1 (BoHV-1) is a promising oncolytic virus with broad antitumor spectrum; however, its oncolytic effects on human lung adenocarcinoma in vivo have not been reported. In this study, we report that BoHV-1 can be used as an oncolytic virus for human [...] Read more.
Bovine herpesvirus 1 (BoHV-1) is a promising oncolytic virus with broad antitumor spectrum; however, its oncolytic effects on human lung adenocarcinoma in vivo have not been reported. In this study, we report that BoHV-1 can be used as an oncolytic virus for human lung adenocarcinoma, and elucidate the underlying mechanism of how BoHV-1 suppresses tumor cell proliferation and growth. First, we examined the oncolytic activities of BoHV-1 in human lung adenocarcinoma A549 cells. BoHV-1 infection reduced the protein levels of histone deacetylases (HDACs), including HDAC1-4 that are promising anti-tumor drug targets. Furthermore, the HDAC inhibitor Trichostatin A (TSA) promoted BoHV-1 infection and exacerbated DNA damage and cytopathology, suggesting a synergy between BoHV-1 and TSA. In the A549 tumor xenograft mouse model, we, for the first time, showed that BoHV-1 can infect tumor and suppressed tumor growth with a similar high efficacy as the treatment of TSA, and HDACs have potential effects on the virus replication. Taken together, our study demonstrates that BoHV-1 has oncolytic effects against human lung adenocarcinoma in vivo. Full article
(This article belongs to the Special Issue The Role of DNA Damage and Repair in Cancer)
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