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DNA Damage, Genome Instability and Cancer
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DNA Damage, Genome Instability and Cancer

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (15 October 2022) | Viewed by 14783

Special Issue Editor

Dr. Rahul Bhowmick

E-Mail Website
Guest Editor
Center for Chromosome Stability and Center for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen N, Denmark
Interests: DNA damage; replication stress; fragile sites; genome instability; aneuploidy; oncogene activation

Special Issue Information

Dear Colleagues,

The propagation of all forms of life depends on the ability to form two cells from one during the process of cell division. This cell duplication requires billions of nucleotides to be accurately copied during the process of DNA replication. Failure to undertake or regulate these processes can lead to the formation of chromosomal breaks or rearrangements, and to the mis-segregation of chromosomes (leading to aneuploidy—an incorrect number of chromosomes). This chromosomal instability or genome instability is a characteristic of almost all human cancers, but the molecular basis of this instability in the context of tumorigenesis is still poorly understood. It is proposed that genome instability promotes tumorigenesis and genetic heterogeneity within tumour cells, thus generating cancer cell variants that are refractory to therapies. Understanding the causes and consequences of genome instability will not only help us to understand the tumorigenesis process but might enlighten new avenues of targeted cancer therapy.

The aim of this Special Issue is not only to focus on the novel mechanisms/pathways employed by cells to maintain genome stability but also to provide novel insights into the roles of genome instability as a driver of tumorigenesis. Topics to be addressed include but are not limited to DNA damage repair, replication stress, cell cycle regulation, oncogene activation, chromosome segregation, fragile sites, and aneuploidy in relation to genome stability maintenance. Overall, this issue will focus on genome stability maintenance and its crucial role in human diseases such as cancer.

Dr. Rahul Bhowmick
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. Genes is an international peer-reviewed open access monthly 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 2600 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 damage
  • rare/common fragile sites
  • replication stress
  • genome instability
  • aneuploidy
  • oncogene activation

Published Papers (6 papers)

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Research

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8 pages, 606 KiB  
Article
Impact of Methionine Synthase Reductase Polymorphisms in Chronic Myeloid Leukemia Patients
by Abozer Y. Elderdery, Entesar M. Tebein, Fawaz O. Alenazy, Ahmed M. E. Elkhalifa, Manar G. Shalabi, Anass M. Abbas, Hassan H. Alhassan, Chand B. Davuljigari and Jeremy Mills
Genes 2022, 13(10), 1729; https://doi.org/10.3390/genes13101729 - 26 Sep 2022
Cited by 3 | Viewed by 1442
Abstract
Introduction： Metabolism methionine and of folate play a vital function in cellular methylation reactions, DNA synthesis and epigenetic process.However, polymorphisms of methionine have received much attention in recent medical genetics research. Objectives: To ascertain whether the common polymorphisms of the MTRR (Methionine [...] Read more.
Introduction： Metabolism methionine and of folate play a vital function in cellular methylation reactions, DNA synthesis and epigenetic process.However, polymorphisms of methionine have received much attention in recent medical genetics research. Objectives: To ascertain whether the common polymorphisms of the MTRR (Methionine Synthase Reductase) A66G gene could play a role in affecting susceptibility to Chronic Myeloid Leukemia (CML) in Sudanese individuals. Methods: In a case-controlled study, we extracted and analyzed DNA from 200 CML patients and 100 healthy control subjects by the PCR-RFLP method. Results: We found no significant difference in age orgender between the patient group and controls. The MTRR A66G genotypes were distributed based on the Hardy-Weinberg equilibrium (p > 0.05). The variation of MTRR A66G was less significantly frequent in cases with CML (68.35%) than in controls (87%) (OR = 0.146, 95% CI = 0.162–0.662, p < 0.002). Additionally, AG and GG genotypes and G allele were reducing the CML risk (Odds ratio [OR] = 0.365; 95% CI [0.179–0.746]; p = 0.006; OR = 0.292; 95% CI [0.145–0.590]; p = 0.001 and OR = 0.146; 95% CI [0.162–0.662]; p = 0.002 and OR = 2.0; 95% CI [1.3853–2.817]; respectively, (p = 0.000)). Conclusions: Our data demonstrated that heterozygous and homozygous mutant genotypes of MTRR polymorphisms were associated with decreased risk of developing CML in the Sudanese population. Full article
(This article belongs to the Special Issue DNA Damage, Genome Instability and Cancer)
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13 pages, 3494 KiB  
Article
Cdh1 Deficiency Sensitizes TNBC Cells to PARP Inhibitors
by Junjun Li, Mengjiao Lan, Jin Peng, Qunli Xiong, Yongfeng Xu, Yang Yang, Ying Zhou, Jinlu Liu, Zhu Zeng, Xiaojuan Yang, Zhiwei Zhang, Pumin Zhang, Qing Zhu and Wei Wu
Genes 2022, 13(5), 803; https://doi.org/10.3390/genes13050803 - 30 Apr 2022
Cited by 2 | Viewed by 2225
Abstract
Triple-negative breast cancer (TNBC) is a type of breast tumor that currently lacks options for targeted therapy. Tremendous effort has been made to identify treatment targets for TNBC. Here, we report that the expression level of anaphase promoting complex (APC) coactivator Cdh1 in [...] Read more.
Triple-negative breast cancer (TNBC) is a type of breast tumor that currently lacks options for targeted therapy. Tremendous effort has been made to identify treatment targets for TNBC. Here, we report that the expression level of anaphase promoting complex (APC) coactivator Cdh1 in TNBC is elevated compared to that in the adjacent healthy tissues, and high levels of Cdh1 expression are correlated with poor prognoses, suggesting that Cdh1 contributes to the progression of TNBC. Interfering with the function of Cdh1 can potentiate the cytotoxic effects of PARP inhibitors against BRCA-deficient and BRCA-proficient TNBC cells through inducing DNA damage, checkpoint activation, cell cycle arrest, and apoptosis. Further investigation reveals that Cdh1 promotes BRCA1 foci formation and prevents untangled DNA entering mitosis in response to PARP inhibition (PARPi) in TNBC cells. Collectively, these results suggest that APC/Cdh1 is a potential molecular target for PARPi-based therapies against TNBCs. Full article
(This article belongs to the Special Issue DNA Damage, Genome Instability and Cancer)
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Review

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19 pages, 808 KiB  
Review
Small Non-Coding RNAs in Human Cancer
by Qunli Xiong, Yaguang Zhang, Junjun Li and Qing Zhu
Genes 2022, 13(11), 2072; https://doi.org/10.3390/genes13112072 - 9 Nov 2022
Cited by 16 | Viewed by 2365
Abstract
Small non-coding RNAs are widespread in the biological world and have been extensively explored over the past decades. Their fundamental roles in human health and disease are increasingly appreciated. Furthermore, a growing number of studies have investigated the functions of small non-coding RNAs [...] Read more.
Small non-coding RNAs are widespread in the biological world and have been extensively explored over the past decades. Their fundamental roles in human health and disease are increasingly appreciated. Furthermore, a growing number of studies have investigated the functions of small non-coding RNAs in cancer initiation and progression. In this review, we provide an overview of the biogenesis of small non-coding RNAs with a focus on microRNAs, PIWI-interacting RNAs, and a new class of tRNA-derived small RNAs. We discuss their biological functions in human cancer and highlight their clinical application as molecular biomarkers or therapeutic targets. Full article
(This article belongs to the Special Issue DNA Damage, Genome Instability and Cancer)
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20 pages, 3242 KiB  
Review
From Processivity to Genome Maintenance: The Many Roles of Sliding Clamps
by Meenakshi Mulye, Manika Indrajit Singh and Vikas Jain
Genes 2022, 13(11), 2058; https://doi.org/10.3390/genes13112058 - 7 Nov 2022
Cited by 4 | Viewed by 2682
Abstract
Sliding clamps play a pivotal role in the process of replication by increasing the processivity of the replicative polymerase. They also serve as an interacting platform for a plethora of other proteins, which have an important role in other DNA metabolic processes, including [...] Read more.
Sliding clamps play a pivotal role in the process of replication by increasing the processivity of the replicative polymerase. They also serve as an interacting platform for a plethora of other proteins, which have an important role in other DNA metabolic processes, including DNA repair. In other words, clamps have evolved, as has been correctly referred to, into a mobile “tool-belt” on the DNA, and provide a platform for several proteins that are involved in maintaining genome integrity. Because of the central role played by the sliding clamp in various processes, its study becomes essential and relevant in understanding these processes and exploring the protein as an important drug target. In this review, we provide an updated report on the functioning, interactions, and moonlighting roles of the sliding clamps in various organisms and its utilization as a drug target. Full article
(This article belongs to the Special Issue DNA Damage, Genome Instability and Cancer)
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17 pages, 2413 KiB  
Review
SPOP in Cancer: Phenomena, Mechanisms and Its Role in Therapeutic Implications
by Xiaojuan Yang and Qing Zhu
Genes 2022, 13(11), 2051; https://doi.org/10.3390/genes13112051 - 7 Nov 2022
Cited by 5 | Viewed by 2575
Abstract
Speckle-type POZ (pox virus and zinc finger protein) protein (SPOP) is a cullin 3-based E3 ubiquitin ligase adaptor protein that plays a crucial role in ubiquitin-mediated protein degradation. Recently, SPOP has attracted major research attention as it is frequently mutated in a range [...] Read more.
Speckle-type POZ (pox virus and zinc finger protein) protein (SPOP) is a cullin 3-based E3 ubiquitin ligase adaptor protein that plays a crucial role in ubiquitin-mediated protein degradation. Recently, SPOP has attracted major research attention as it is frequently mutated in a range of cancers, highlighting pleiotropic tumorigenic effects and associations with treatment resistance. Structurally, SPOP contains a functionally critical N-terminal meprin and TRAF homology (MATH) domain for many SPOP substrates. SPOP has two other domains, including the internal Bric-a-brac-Tramtrack/Broad (BTB) domain, which is linked with SPOP dimerization and binding to cullin3, and a C-terminal nuclear localization sequence (NLS). The dysregulation of SPOP-mediated proteolysis is associated with the development and progression of different cancers since abnormalities in SPOP function dysregulate cellular signaling pathways by targeting oncoproteins or tumor suppressors in a tumor-specific manner. SPOP is also involved in genome stability through its role in the DNA damage response and DNA replication. More recently, studies have shown that the expression of SPOP can be modulated in various ways. In this review, we summarize the current understanding of SPOP’s functions in cancer and discuss how to design a rational therapeutic target. Full article
(This article belongs to the Special Issue DNA Damage, Genome Instability and Cancer)
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31 pages, 1790 KiB  
Review
Translational Regulation by eIFs and RNA Modifications in Cancer
by Linzhu Zhang, Yaguang Zhang, Su Zhang, Lei Qiu, Yang Zhang, Ying Zhou, Junhong Han and Jiang Xie
Genes 2022, 13(11), 2050; https://doi.org/10.3390/genes13112050 - 6 Nov 2022
Cited by 5 | Viewed by 2713
Abstract
Translation is a fundamental process in all living organisms that involves the decoding of genetic information in mRNA by ribosomes and translation factors. The dysregulation of mRNA translation is a common feature of tumorigenesis. Protein expression reflects the total outcome of multiple regulatory [...] Read more.
Translation is a fundamental process in all living organisms that involves the decoding of genetic information in mRNA by ribosomes and translation factors. The dysregulation of mRNA translation is a common feature of tumorigenesis. Protein expression reflects the total outcome of multiple regulatory mechanisms that change the metabolism of mRNA pathways from synthesis to degradation. Accumulated evidence has clarified the role of an increasing amount of mRNA modifications at each phase of the pathway, resulting in translational output. Translation machinery is directly affected by mRNA modifications, influencing translation initiation, elongation, and termination or altering mRNA abundance and subcellular localization. In this review, we focus on the translation initiation factors associated with cancer as well as several important RNA modifications, for which we describe their association with cancer. Full article
(This article belongs to the Special Issue DNA Damage, Genome Instability and Cancer)
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