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https://www.readbyqxmd.com/read/29433451/nbs1-rs2735383-polymorphism-is-associated-with-an-increased-risk-of-laryngeal-carcinoma
#1
Xinmei Hu, Juan Liao, Huiliu Zhao, Feng Chen, Xuefeng Zhu, Jiangheng Li, Qingqing Nong
BACKGROUND: Nijmegen breakage syndrome 1 (NBS1), as a key protein in the DNA double-strand breaks (DSBs) repair pathway, plays an important role in maintaining genomic stability. Although single nucleotide polymorphisms (SNPs) in NBS1 have frequently been studied in multiple cancers, the relationships of two functional NBS1 polymorphisms (rs2735383 and rs1805794) with laryngeal carcinoma are yet unclear. Therefore, in the present study, we performed a case-control study including 342 cases and 345 controls to analyze the associations between two polymorphisms of NBS1 and the risk of laryngeal carcinoma...
February 12, 2018: BMC Cancer
https://www.readbyqxmd.com/read/29432179/parp-1-dependent-recruitment-of-cold-inducible-rna-binding-protein-promotes-double-strand-break-repair-and-genome-stability
#2
Jung-Kuei Chen, Wen-Ling Lin, Zhang Chen, Hung-Wen Liu
Maintenance of genome integrity is critical for both faithful propagation of genetic information and prevention of mutagenesis induced by various DNA damage events. Here we report cold-inducible RNA-binding protein (CIRBP) as a newly identified key regulator in DNA double-strand break (DSB) repair. On DNA damage, CIRBP temporarily accumulates at the damaged regions and is poly(ADP ribosyl)ated by poly(ADP ribose) polymerase-1 (PARP-1). Its dissociation from the sites of damage may depend on its phosphorylation status as mediated by phosphatidylinositol 3-kinase-related kinases...
February 5, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29416357/a-non-synonymous-polymorphism-in-nbs1-is-associated-with-progression-from-chronic-hepatitis-b-virus-infection-to-hepatocellular-carcinoma-in-a-chinese-population
#3
Ya'nan Zhen, Ruixue Xiao, Xing Chen, Changjin Yuan, Yanlai Sun, Jie Li
Purpose: Nijmegen breakage syndrome 1 (NBS1) has a vital role in DNA double-strand break (DSB) repair, functioning as a sensor to identify and repair DNA damage and maintaining genomic stability by participating in the intra-S-phase checkpoint. Polymorphisms of NBS1 have been investigated in multiple cancers with variable results. To our best knowledge, no previous study has focused on the association between NBS1 single-nucleotide polymorphisms (SNPs) and hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC)...
2018: OncoTargets and Therapy
https://www.readbyqxmd.com/read/29396424/inactivation-of-ribosomal-protein-s27-like-confers-radiosensitivity-via-the-mdm2-p53-and-mdm2-mrn-atm-axes
#4
Yongchao Zhao, Mingjia Tan, Xia Liu, Xiufang Xiong, Yi Sun
RPS27L (ribosomal protein S27-like) is an evolutionarily conserved ribosomal protein and a direct p53 target. We recently reported that Rps27l disruption triggers ribosomal stress to induce p53, causing postnatal death, which can be rescued by Trp53 +/- . Whether and how Rps27l modulates radiosensitivity is unknown. Here we report that Rps27l -/- ; Trp53 +/- mice are extremely sensitive to radiation due to reduced proliferation and massive induction of apoptosis in radiation-sensitive organs. Mechanistically, the radiation sensitivity is mediated by two signaling pathways: (1) activated p53 pathway due to imbalanced Mdm2/Mdm4 levels and reduced E3 ligase activity; and (2) reduced DNA damage response due to reduced MRN/Atm signal as a result of elevated Mdm2 binding of Nbs1 to inhibit Nbs1-Atm binding and subsequent Atm activation...
February 2, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29368209/breast-cancer-risk-associated-with-genes-encoding-dna-repair-mrn-complex-a-study-from-punjab-pakistan
#5
Rabbia Tariq Khan, Ayesha Siddique, Naeem Shahid, Samina Khokher, Warda Fatima
BACKGROUND: Variants of DNA repair genes are extensively reported to cause genetic instability and increase the risk of breast cancer. In combination with NBS1, MRE11 and RAD50 constitute an MRN (MRE11-RAD50-NBS1) complex that repairs DNA damage. However, certain genetic alterations in MRE11 and RAD50 produce abnormal protein that affects the repairing process and may result in malignancy. We aimed to investigate the association of MRE11 and RAD50 polymorphisms with breast risk in the female population of Punjab, Pakistan...
January 24, 2018: Breast Cancer: the Journal of the Japanese Breast Cancer Society
https://www.readbyqxmd.com/read/29361783/localization-microscopy-analyses-of-mre11-clusters-in-3d-conserved-cell-nuclei-of-different-cell-lines
#6
Marion Eryilmaz, Eberhard Schmitt, Matthias Krufczik, Franziska Theda, Jin-Ho Lee, Christoph Cremer, Felix Bestvater, Wladimir Schaufler, Michael Hausmann, Georg Hildenbrand
In radiation biophysics, it is a subject of nowadays research to investigate DNA strand break repair in detail after damage induction by ionizing radiation. It is a subject of debate as to what makes up the cell's decision to use a certain repair pathway and how the repair machinery recruited in repair foci is spatially and temporarily organized. Single-molecule localization microscopy (SMLM) allows super-resolution analysis by precise localization of single fluorescent molecule tags, resulting in nuclear structure analysis with a spatial resolution in the 10 nm regime...
January 22, 2018: Cancers
https://www.readbyqxmd.com/read/29322791/targeting-rad50-increases-sensitivity-to-radiotherapy-in-colorectal-cancer-cells
#7
C Chen, Y Wang, J F Mei, S S Li, H X Xu, H P Xiong, X H Wang, X He
Radiotherapy resistance remains the major factor limiting the radiotherapy efficacy in colorectal cancer. The Mre11-RAD50-Nbs1 (MRN) complex is known to play a critical role in the DNA double strand breaks (DSBs) repair pathways and thus facilitates radioresistance. Targeting MRN function can sensitize cancer cells to irradiation in some malignancies. In this study, we stably knocked down RAD50 protein in colorectal cancer (CRC) cell lines, HCT116 and DLD1, and evaluated their response to irradiation as well as the DSB repair dynamics...
2018: Neoplasma
https://www.readbyqxmd.com/read/29317520/atm-directs-dna-damage-responses-and-proteostasis-via-genetically-separable-pathways
#8
Ji-Hoon Lee, Michael R Mand, Chung-Hsuan Kao, Yi Zhou, Seung W Ryu, Alicia L Richards, Joshua J Coon, Tanya T Paull
The protein kinase ATM is a master regulator of the DNA damage response but also responds directly to oxidative stress. Loss of ATM causes ataxia telangiectasia, a neurodegenerative disorder with pleiotropic symptoms that include cerebellar dysfunction, cancer, diabetes, and premature aging. We genetically separated the activation of ATM by DNA damage from that by oxidative stress using separation-of-function mutations. We found that deficient activation of ATM by the Mre11-Rad50-Nbs1 complex and DNA double-strand breaks resulted in loss of cell viability, checkpoint activation, and DNA end resection in response to DNA damage...
January 9, 2018: Science Signaling
https://www.readbyqxmd.com/read/29297932/inhibition-of-novel-gcn5-atm-axis-restricts-the-onset-of-acquired-drug-resistance-in-leukemia
#9
Sameer Salunkhe, Saket V Mishra, Jyothi Nair, Samadri Ghosh, Neha Choudhary, Ekjot Kaur, Sanket Shah, Ketaki Patkar, Dev Anand, Navin Khattry, Syed K Hasan, Shilpee Dutt
Leukemia is majorly treated by topoisomerase inhibitors that induce DNA double strand breaks (DSB) resulting in cell death. Consequently, modulation of DSB repair pathway renders leukemic cells resistant to therapy. Since we do not fully understand the regulation of DSB repair acquired by resistant cells, targeting these cells has been a challenge. Here we investigated the regulation of DSB repair pathway in Early Drug Resistant Population (EDRP) and Late Drug Resistant Population (LDRP). We found that doxorubicin induced equal DSBs in parent and EDRP cells however; cell death is induced only in the parent cells...
January 3, 2018: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/29285240/molecular-basis-for-the-dna-damage-induction-and-anticancer-activity-of-asymmetrically-substituted-anthrapyridazone-pdz-7
#10
Majus Misiak, Mateusz Heldt, Marlena Szeligowska, Stefania Mazzini, Leonardo Scaglioni, Grzegorz J Grabe, Marcin Serocki, Jan Lica, Marta Switalska, Joanna Wietrzyk, Giovanni L Beretta, Paola Perego, Dominik Zietkowski, Maciej Baginski, Edward Borowski, Andrzej Skladanowski
Anthrapyridazones, imino analogues of anthraquinone, constitute a family of compounds with remarkable anti-cancer activity. To date, over 20 derivatives were studied, of which most displayed nanomolar cytotoxicity towards broad spectrum of cancer cells, including breast, prostate and leukemic ones. BS-154, the most potent derivative, had IC50 values close to 1 nM, however, it was toxic in animal studies. Here, we characterize another anthrapyridazone, PDZ-7, which retains high cytotoxicity while being well tolerated in mice...
December 1, 2017: Oncotarget
https://www.readbyqxmd.com/read/29217481/dna-damage-and-repair-proteins-in-cellular-response-to-sulfur-mustard-in-iranian-veterans-more-than-two-decades-after-exposure
#11
Shahriar Khateri, Mahdi Balali-Mood, Peter Blain, Faith Williams, Paul Jowsey, Mohammad Reza Soroush, Effat Behravan, Mahmood Sadeghi
Delayed effects of sulfur mustard (SM) exposure on the levels of five important damage/repair proteins were investigated in 40 SM-exposed veterans of Iran-Iraq war and 35 unexposed controls. A major DNA damage biomarker protein - phosphorylated H2AX - along with four DNA repair proteins in cell response to the genome damage MRE11, NBS1, RAD51, and XPA were evaluated in blood lymphocytes from the veterans and controls using western blotting. Mean levels of XPA, MRE11, RAD51 and NBS1 were lower in SM-exposed patients and the decrease in NBS1 was significant...
December 4, 2017: Toxicology Letters
https://www.readbyqxmd.com/read/29200877/microtubule-targeting-agents-can-sensitize-cancer-cells-to-ionizing-radiation-by-an-interphase-based-mechanism
#12
Daniel Markowitz, Grace Ha, Rosamaria Ruggieri, Marc Symons
Background: The cytotoxic effects of microtubule-targeting agents (MTAs) are often attributed to targeted effects on mitotic cells. In clinical practice, MTAs are combined with DNA-damaging agents such as ionizing radiation (IR) with the rationale that mitotic cells are highly sensitive to DNA damage. In contrast, recent studies suggest that MTAs synergize with IR by interfering with the trafficking of DNA damage response (DDR) proteins during interphase. These studies, however, have yet to demonstrate the functional consequences of interfering with interphase microtubules in the presence of IR...
2017: OncoTargets and Therapy
https://www.readbyqxmd.com/read/29180822/damage-induced-lncrnas-control-the-dna-damage-response-through-interaction-with-ddrnas-at-individual-double-strand-breaks
#13
Flavia Michelini, Sethuramasundaram Pitchiaya, Valerio Vitelli, Sheetal Sharma, Ubaldo Gioia, Fabio Pessina, Matteo Cabrini, Yejun Wang, Ilaria Capozzo, Fabio Iannelli, Valentina Matti, Sofia Francia, G V Shivashankar, Nils G Walter, Fabrizio d'Adda di Fagagna
The DNA damage response (DDR) preserves genomic integrity. Small non-coding RNAs termed DDRNAs are generated at DNA double-strand breaks (DSBs) and are critical for DDR activation. Here we show that active DDRNAs specifically localize to their damaged homologous genomic sites in a transcription-dependent manner. Following DNA damage, RNA polymerase II (RNAPII) binds to the MRE11-RAD50-NBS1 complex, is recruited to DSBs and synthesizes damage-induced long non-coding RNAs (dilncRNAs) from and towards DNA ends...
December 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/29165875/4%C3%AE-hydroxywithanolide-e-selectively-induces-oxidative-dna-damage-for-selective-killing-of-oral-cancer-cells
#14
Jen-Yang Tang, Hurng-Wern Huang, Hui-Ru Wang, Ya-Ching Chan, Jo-Wen Haung, Chih-Wen Shu, Yang-Chang Wu, Hsueh-Wei Chang
Reactive oxygen species (ROS) induction had been previously reported in 4β-hydroxywithanolide (4βHWE)-induced selective killing of oral cancer cells, but the mechanism involving ROS and the DNA damage effect remain unclear. This study explores the role of ROS and oxidative DNA damage of 4βHWE in the selective killing of oral cancer cells. Changes in cell viability, morphology, ROS, DNA double strand break (DSB) signaling (γH2AX foci in immunofluorescence and DSB signaling in western blotting), and oxidative DNA damage (8-oxo-2'deoxyguanosine [8-oxodG]) were detected in 4βHWE-treated oral cancer (Ca9-22) and/or normal (HGF-1) cells...
November 22, 2017: Environmental Toxicology
https://www.readbyqxmd.com/read/29101112/prostate-cancer-germline-variations-and-implications-for-screening-and-treatment
#15
Alexander Dias, Zsofia Kote-Jarai, Christos Mikropoulos, Ros Eeles
Prostate cancer (PCa) is a highly heritable disease, and rapid evolution of sequencing technologies has enabled marked progression of our understanding of its genetic inheritance. A complex polygenic model that involves common low-penetrance susceptibility alleles causing individually small but cumulatively significant risk and rarer genetic variants causing greater risk represent the current most accepted model. Through genome-wide association studies, more than 100 single-nucleotide polymorphisms (SNPs) associated with PCa risk have been identified...
November 3, 2017: Cold Spring Harbor Perspectives in Medicine
https://www.readbyqxmd.com/read/29065514/the-role-of-mdm2-in-promoting-genome-stability-versus-instability
#16
REVIEW
M Reza Saadatzadeh, Adily N Elmi, Pankita H Pandya, Khadijeh Bijangi-Vishehsaraei, Jixin Ding, Christopher W Stamatkin, Aaron A Cohen-Gadol, Karen E Pollok
In cancer, the mouse double minute 2 (MDM2) is an oncoprotein that contributes to the promotion of cell growth, survival, invasion, and therapeutic resistance. The impact of MDM2 on cell survival versus cell death is complex and dependent on levels of MDM2 isoforms, p53 status, and cellular context. Extensive investigations have demonstrated that MDM2 protein-protein interactions with p53 and other p53 family members (p63 and p73) block their ability to function as transcription factors that regulate cell growth and survival...
October 23, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29024686/increased-age-adjusted-hazard-of-death-associated-with-a-common-single-nucleotide-polymorphism-of-the-human-rad52-gene-in-a-cardiovascular-cohort
#17
Peter Lenart, Filip Zlámal, Jan Machal, Ota Hlinomaz, Ladislav Groch, Julie Bienertová-Vašků
Aging may be characterized as the progressive increase of the risk of death caused by a decrease of almost all bodily functions. While a great number of model organism studies have established the role of DNA double strand breaks (DSBs) as one of the main causes of aging, few studies have examined whether common polymorphisms in human DSB repair genes influence aging and mortality. More importantly, to the best of our knowledge, no longitudinal study has thus far examined the link between polymorphisms in DSB repair and the risk of death...
October 2017: Mechanisms of Ageing and Development
https://www.readbyqxmd.com/read/29018935/a-curious-new-role-for-mrn-in-schizosaccharomyces-pombe-non-homologous-end-joining
#18
REVIEW
Kurt W Runge, Yanhui Li
Chromosomal breaks can be healed by several repair processes, including one called non-homologous end-joining (NHEJ) where the two broken ends are ligated together with a loss of 0-5 bp of DNA. The protein requirements for NHEJ of cut DNA ends in the budding yeast Saccharomyces cerevisiae include its version of the Mre11-Rad50-Nbs1 (MRN) complex. In contrast, the fission yeast Schizosaccharomyces pombe and mammalian cells do not require MRN for this process. Recent work in S. pombe used transposon excision to generate breaks that were capped by DNA hairpins, which must be opened to produce ligatable ends...
October 10, 2017: Current Genetics
https://www.readbyqxmd.com/read/28976141/population-specific-genetic-variation-at-microrna-629-binding-site-in-the-3-utr-of-nbs1-gene-in-prostate-cancer-patients
#19
Ammad Ahmad Farooqi, Syed M Kamran Majeed, Qaisar Mansoor, Muhammad Ismail
OBJECTIVE: Prostate cancer is a genomically complex disease and recently emerging scientific evidence is adding new pieces of information into existing pool of knowledge of oncology. Prostate cancer cells tactfully rewire signaling cascades in presence or absence of androgen. We do not have finer proteome and genome based patient related information of our cancer patients. METHODOLOGY: In the present laboratory research, we studied 3' UTR C/T and A/G polymorphism in NBS1 gene in 100 prostate cancer patients and 100 healthy individuals without any previous clinical history, using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis...
September 2017: Journal of Experimental Therapeutics & Oncology
https://www.readbyqxmd.com/read/28967905/akt-overactivation-can-suppress-dna-repair-via-p70s6-kinase-dependent-downregulation-of-mre11
#20
D Piscitello, D Varshney, S Lilla, M G Vizioli, C Reid, V Gorbunova, A Seluanov, D A Gillespie, P D Adams
Deregulated AKT kinase activity due to PTEN deficiency in cancer cells contributes to oncogenesis by incompletely understood mechanisms. Here, we show that PTEN deletion in HCT116 and DLD1 colon carcinoma cells leads to suppression of CHK1 and CHK2 activation in response to irradiation, impaired G2 checkpoint proficiency and radiosensitization. These defects are associated with reduced expression of MRE11, RAD50 and NBS1, components of the apical MRE11/RAD50/NBS1 (MRN) DNA damage response complex. Consistent with reduced MRN complex function, PTEN-deficient cells fail to resect DNA double-strand breaks efficiently after irradiation and show greatly diminished proficiency for DNA repair via the error-free homologous recombination (HR) repair pathway...
October 2, 2017: Oncogene
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