Review
Genetics & Heredity
Apfrida Kendek, Marieke R. Wensveen, Aniek Janssen
Summary: The eukaryotic nucleus is constantly exposed to sources causing DNA breaks, requiring dedicated nuclear machinery for faithful repair. DNA is packaged into various chromatin domains with specific molecular properties regulating gene expression and nuclear structure maintenance. Different chromatin environments demand tailored responses to DNA damage.
Review
Oncology
Angelos Papaspyropoulos, Orsalia Hazapis, Nefeli Lagopati, Aikaterini Polyzou, Anastasios D. Papanastasiou, Michalis Liontos, Vassilis G. Gorgoulis, Athanassios Kotsinas
Summary: The text highlights the underappreciated role of non-coding RNAs, particularly circular RNAs, in the DNA damage response and repair network. It emphasizes the importance of further research in this area for potential therapeutic opportunities, while also acknowledging the lack of detailed understanding of the properties and functional roles of these molecules.
Review
Cell Biology
Lia Yedidia-Aryeh, Michal Goldberg
Summary: Cancer development is often associated with impaired DNA repair and DNA damage signaling pathways. Estrogen has a regulatory role in the repair and cellular response to DNA double-strand breaks. There is a complex interplay between the cellular DNA damage response and the actions of estrogen, which may contribute to the development of estrogen-dependent cancers.
Review
Cell Biology
Ksenia G. Kolobynina, Alexander Rapp, M. Cristina Cardoso
Summary: Chromatin serves as the background for all DNA-based molecular processes in the cell nucleus. The initial chromatin structure at the site of DNA damage determines lesion generation and activation of the DNA damage response pathway. Ubiquitination, as an important chromatin post-translational modification, is involved in chromatin changes at the damaged site and throughout the genome.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2022)
Review
Cell Biology
Angelos Papaspyropoulos, Nefeli Lagopati, Ioanna Mourkioti, Andriani Angelopoulou, Spyridon Kyriazis, Michalis Liontos, Vassilis Gorgoulis, Athanassios Kotsinas
Summary: Protection of genome integrity is crucial, and eukaryotes have developed NHEJ and HR pathways to repair DSBs. Recent research has identified non-coding RNAs, especially lncRNAs, as key players in these pathways with therapeutic potential.
Article
Engineering, Multidisciplinary
Kamila Sofi, Michal Ciesla, Jakub Barbasz, Natalia Wilkosz, Ewelina Lipiec, Marek Szymonski, Piotr Bialas
Summary: DNA is susceptible to various damaging factors, which can cause single- or double-strand breaks. Atomic force microscopy is used to determine the length of DNA fragments deposited on surfaces and quantify double-strand breaks. To overcome the underestimation caused by image resolution, a new methodology based on statistics of DNA fragment length is proposed, along with software for automatic calculation of double-strand breaks. The method is applied to characterize DNA plasmid fragmentation caused by the anticancer chemotherapeutic drug bleomycin.
Review
Cell Biology
Zulong Chen, Jessica K. Tyler
Summary: This review presents our current understanding of how DNA double-strand break repair pathways are employed in various chromatin landscapes, with a focus on the impact of histone post-translational modifications and damage-induced chromatin modifications on repair pathway choice. The potential roles of RNA transcripts from DSBs in actively transcribed regions in regulating repair pathway choice are also discussed.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2022)
Review
Environmental Sciences
Ericka Marel Quezada-Maldonado, Yesennia Sanchez-Perez, Yolanda I. Chirino, Claudia M. Garcia-Cuellar
Summary: This study analyzed the types of DNA damage and alterations in DNA repair pathways induced by PM exposure, showing that PM mainly causes oxidative stress and DNA damage through the formation of DNA adducts and DSBs, as well as deregulates the protein expression in DNA repair pathways. However, there are still limitations in the knowledge about the effects of PM on DNA repair pathways, and further research is needed to deepen our understanding.
ENVIRONMENTAL POLLUTION
(2021)
Article
Oncology
Shiyu Wang, Yanan Wang, Xiangnan Liu, Yongbin Yang, Sufang Wu, Yuan Liu
Summary: This study investigated the radiotherapy sensitization mechanism in cervical cancer through the exploration of Sulforaphane (SFN) as a potential sensitizer. SFN treatment inhibited the survival of cervical cancer cells and resulted in the suppression of the homologous recombination pathway, thereby enhancing the sensitivity of radiotherapy. LATS2 was identified as a downstream target of SFN treatment and played a crucial role in the SFN-facilitated radiotherapy sensitization.
Article
Biochemistry & Molecular Biology
Dimitra T. Stefanou, Marousa Kouvela, Dimitris Stellas, Konstantinos Voutetakis, Olga Papadodima, Konstantinos Syrigos, Vassilis L. Souliotis
Summary: The deregulated DNA damage response network is associated with the onset and progression of lung cancer. This study found that lung cancer patients have higher levels of endogenous DNA damage, which may be caused by oxidative stress and defective DNA repair mechanisms. The findings suggest that oxidative stress and DDR-related aberrations contribute to the accumulation of endogenous DNA damage in lung cancer patients.
Article
Cell Biology
Md Akram Hossain, Yunfeng Lin, Garrett Driscoll, Jia Li, Anne McMahon, Joshua Matos, Haichao Zhao, Daisuke Tsuchimoto, Yusaku Nakabeppu, Jianjun Zhao, Shan Yan
Summary: APE2 is essential for activating the ATR DDR pathway in response to various stressful conditions in Xenopus laevis egg extracts and human pancreatic cancer cells. Inhibition of APE2 leads to increased DNA damage and sensitizes cancer cells to chemotherapy drugs, indicating its crucial role in maintaining genome integrity.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Review
Biochemistry & Molecular Biology
Julie A. Klaric, Stas Wust, Stephanie Panier
Summary: DNA double-strand breaks are cytotoxic DNA lesions that trigger a complex signaling response in cells to protect genomic stability. RNA-binding proteins play a crucial role in this response, with functions extending beyond gene expression to participate in DNA repair and signal transduction processes at damaged chromatin. Their involvement in the DSB response also has implications for genome instability and age-related diseases like cancer and neurodegeneration.
FRONTIERS IN MOLECULAR BIOSCIENCES
(2021)
Article
Cell Biology
Nathalie Berthault, Ptissam Bergam, Floriane Pereira, Pierre-Marie Girard, Marie Dutreix
Summary: AsiDNA, a DNA repair inhibitor, disrupts DNA double-strand breaks (DSB) repair pathways to sensitize tumors to DNA damaging therapies. It activates ATM and PARP in the cytoplasm, preventing the formation of repair foci on irradiation-induced damage. AsiDNA also associates with DNA-PK in the nucleus to inhibit the recruitment of repair enzymes at damage sites.
Article
Cell Biology
Xiaoqing Li, Dexuan Gao, Fei Shen, Hengrui Chen, Zhuqiang Zhang, Chao He, Aidi Gao, Yue Lang, Xiaozhong Zhu, Jundong Zhou, Zeng-Fu Shang, Wei-Qun Ding, Ji Zhu
Summary: Radiotherapy resistance is a crucial challenge in managing esophageal squamous carcinoma (ESCC), but the factors and molecular mechanisms underlying ESCC resistance to radiotherapy are not fully understood. This study found that high expression of DNA polymerase iota (POLI) is associated with shorter survival in ESCC patients receiving radiotherapy. Down-regulating POLI increased ESCC sensitivity to radiation and prolonged DNA damage markers. POLI stabilizes RAD51 protein by competitively binding with E3 ligase XIAP and blocking RAD51's ubiquitination, leading to the activation of the GAS signaling pathway. These findings provide new insights into the role of POLI in ESCC radioresistance by stabilizing RAD51 protein.
CELL DEATH DISCOVERY
(2023)
Review
Genetics & Heredity
Fabiola Garcia Fernandez, Emmanuelle Fabre
Summary: Research has shown that chromatin mobility is affected by DNA damage. In the case of double-strand breaks, the mobility of chromatin at the break site is severely affected, while that of other chromosomes is affected to a lesser extent.
Review
Medicine, Research & Experimental
Rui Ma, Yili Feng, Shuang Lin, Jiang Chen, Hui Lin, Xiao Liang, Heming Zheng, Xiujun Cai
JOURNAL OF TRANSLATIONAL MEDICINE
(2015)
Review
Medicine, General & Internal
Jia-Cheng Tang, Yi-Li Feng, Xiao Liang, Xiu-Jun Cai
CHINESE MEDICAL JOURNAL
(2016)
Review
Biochemistry & Molecular Biology
Jia-Cheng Tang, Yi-Li Feng, Tao Guo, An-Yong Xie, Xiu-Jun Cai
CELL AND BIOSCIENCE
(2016)
Article
Biochemistry & Molecular Biology
Yi-Li Feng, Ji-Feng Xiang, Si-Cheng Liu, Tao Guo, Guo-Fang Yan, Ye Feng, Na Kong, Hao-Dan Li, Yang Huang, Hui Lin, Xiu-Jun Cai, An-Yong Xie
NUCLEIC ACIDS RESEARCH
(2017)
Article
Biotechnology & Applied Microbiology
Yi-Li Feng, Wei-Qi Li, Xue-Qian Wu, Jun-Wen Cheng, Su-Yun Ma
BIOCHEMICAL ENGINEERING JOURNAL
(2010)
Article
Chemistry, Applied
Yili Feng, Weiqi Li, Xueqian Wu, Liang He, Suyun Ma
CARBOHYDRATE POLYMERS
(2010)
Article
Biochemistry & Molecular Biology
Yili Feng, Hongxing Wu, Yongxian Xu, Zhengmao Zhang, Ting Liu, Xia Lin, Xin-Hua Feng
JOURNAL OF BIOLOGICAL CHEMISTRY
(2014)
Review
Medicine, Research & Experimental
Liang Shi, Yili Feng, Hui Lin, Rui Ma, Xiujun Cai
JOURNAL OF TRANSLATIONAL MEDICINE
(2014)
Review
Biochemistry & Molecular Biology
Yili Feng, Sicheng Liu, Ruodan Chen, Anyong Xie
Summary: The CRISPR/Cas9 technology is widely used for genome editing, with the variation in target binding affinity and residence time potentially affecting the choice of DSB repair pathway and leading to heterogeneous mutations. This presents an opportunity for optimizing Cas9-based technologies.
JOURNAL OF ZHEJIANG UNIVERSITY-SCIENCE B
(2021)
Article
Cell Biology
Jing Zhang, Yiyang Hong, Zhenyu Liuyang, Haozhe Li, Zhongyang Jiang, Jingjing Tao, Hai Liu, Anyong Xie, Yili Feng, Xingjian Dong, Yihong Wang, Qinghua Dong, Guanyu Wang
Summary: Quercetin can prevent radiation-induced oral mucositis by reducing oxidative stress, inflammation, and DNA damage. It also contributes to ulcer repair and wound healing by promoting cell proliferation and repair mechanisms.
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
(2021)
Article
Multidisciplinary Sciences
Yi-Li Feng, Qian Liu, Ruo-Dan Chen, Si-Cheng Liu, Zhi-Cheng Huang, Kun-Ming Liu, Xiao-Ying Yang, An-Yong Xie
Summary: Analysis of human cancer genome sequences has identified specific mutation characteristics associated with BRCA1-deficient tumors, but the mechanisms behind them are not well understood. In this study, it was found that one-ended DNA double strand breaks (DSBs) converted from CRISPR/Cas9-induced nicks by DNA replication, rather than two-ended DSBs, cause more chromosomal aberrations and micronuclei in Brca1-deficient cells. BRCA1 is required for efficient homologous recombination of these nick-converted DSBs and suppresses bias towards long tract gene conversion and tandem duplication mediated by two-round strand invasion in a replication strand asymmetry. However, abnormal repair of these nick-converted one-ended DSBs, not of two-ended DSBs in Brca1-deficient cells, generates mutational signatures similar to those observed in BRCA1-deficient tumors. These results suggest that DNA nicks play a major role in the mutational signatures associated with BRCA1 deficiency in cancer and shed light on the underlying mechanisms.
NATURE COMMUNICATIONS
(2022)
Article
Biotechnology & Applied Microbiology
Tao Guo, Yi-Li Feng, Jing-Jing Xiao, Qian Liu, Xiu-Na Sun, Ji-Feng Xiang, Na Kong, Si-Cheng Liu, Guo-Qiao Chen, Yue Wang, Meng-Meng Dong, Zhen Cai, Hui Lin, Xiu-Jun Cai, An-Yong Xie