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Dna damage and cancer

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https://www.readbyqxmd.com/read/28750356/combined-calcitriol-and-menadione-reduces-experimental-murine-triple-negative-breast-tumor
#1
Luciana Bohl, Solange Guizzardi, Valeria Rodríguez, Lucila Hinrichsen, Viviana Rozados, David Cremonezzi, Nori Tolosa de Talamoni, Gabriela Picotto
BACKGROUND: Calcitriol (D) or 1,25(OH)2D3 inhibits the growth of several tumor cells including breast cancer cells, by activating cell death pathways. Menadione (MEN), a glutathione-depleting compound, may be used to potentiate the antiproliferative actions of D on cancer cells. We have previously shown in vitro that MEN improved D-induced growth arrest on breast cancer cell lines, inducing oxidative stress and DNA damage via ROS generation. Treatment with MEN+D resulted more effective than D or MEN alone...
July 24, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28750281/heteroleptic-monometallic-and-trimetallic-ruthenium-ii-complexes-incorporating-a-%C3%AF-extended-dipyrrin-ligand-light-activated-reactions-with-the-a549-lung-cancer-cell-line
#2
Shawn Swavey, Krista Morford, Max Tsao, Kristen Comfort, Mary Kate Kilroy
A heteroleptic monometallic ruthenium(II) and a heteroleptic trimetallic ruthenium(II) complex have been synthesized and characterized. Both complexes have an overall 3+ charge, with the charge density greater for the monometallic complex. The electronic spectra of the monometallic ruthenium(II) complex exhibits intense π-π* transitions associated with the bipyridyl groups along with overlapping metal to ligand charge transfer (MLCT) and ligand centered π-π* transitions ranging from 520nm to approximately 600nm...
July 18, 2017: Journal of Inorganic Biochemistry
https://www.readbyqxmd.com/read/28750166/repair-resistant-dna-lesions
#3
Nicholas E Geacintov, Suse Broyde
The eukaryotic global genomic nucleotide excision repair (GG-NER) pathway is the major mechanism that removes most bulky and some non-bulky lesions from cellular DNA. There is growing evidence that certain DNA lesions are repaired slowly, or are entirely resistant to repair in cells, tissues, and in cell extract model assay systems. It is well established that the eukaryotic DNA lesion-sensing proteins do not detect the damaged nucleotide, but recognize the distortions/destabilizations in the native DNA structure caused by the damaged nucleotides...
July 27, 2017: Chemical Research in Toxicology
https://www.readbyqxmd.com/read/28749464/the-cohesin-complex-prevents-myc-induced-replication-stress
#4
Sara Rohban, Aurora Cerutti, Marco J Morelli, Fabrizio d'Adda di Fagagna, Stefano Campaner
The cohesin complex is mutated in cancer and in a number of rare syndromes collectively known as Cohesinopathies. In the latter case, cohesin deficiencies have been linked to transcriptional alterations affecting Myc and its target genes. Here, we set out to understand to what extent the role of cohesins in controlling cell cycle is dependent on Myc expression and activity. Inactivation of the cohesin complex by silencing the RAD21 subunit led to cell cycle arrest due to both transcriptional impairment of Myc target genes and alterations of replication forks, which were fewer and preferentially unidirectional...
July 27, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28748501/a-step-by-step-microrna-guide-to-cancer-development-and-metastasis
#5
REVIEW
Georgios S Markopoulos, Eugenia Roupakia, Maria Tokamani, Evangelia Chavdoula, Maria Hatziapostolou, Christos Polytarchou, Kenneth B Marcu, Athanasios G Papavassiliou, Raphael Sandaltzopoulos, Evangelos Kolettas
BACKGROUND: Cancer is one of the leading causes of mortality. The neoplastic transformation of normal cells to cancer cells is caused by a progressive accumulation of genetic and epigenetic alterations in oncogenes, tumor suppressor genes and epigenetic regulators, providing cells with new properties, collectively known as the hallmarks of cancer. During the process of neoplastic transformation cells progressively acquire novel characteristics such as unlimited growth potential, increased motility and the ability to migrate and invade adjacent tissues, the ability to spread from the tumor of origin to distant sites, and increased resistance to various types of stresses, mostly attributed to the activation of genetic stress-response programs...
July 26, 2017: Cellular Oncology (Dordrecht)
https://www.readbyqxmd.com/read/28747541/obesity-a-serious-etiologic-factor-for-male-subfertility-in-modern-society
#6
Yue Liu, Zhide Ding
Obesity, defined as excessive accumulation of fat in adipose tissue, is a metabolic disorder resulting from behavioral, environmental and heritable causes. Such malfunction increases the risk of developing hypertension, diabetes, cardiovascular disease, respiratory problems, osteoarthritis and cancer. Meanwhile, the negative impact of obesity on male reproduction is gradually being recognized. According to clinical investigations and animal experiments, obesity is correlated with reductions in sperm concentration and motility, increases in sperm DNA damage and changes in reproductive hormonal levels...
July 26, 2017: Reproduction: the Official Journal of the Society for the Study of Fertility
https://www.readbyqxmd.com/read/28747513/repression-of-bet-activity-sensitizes-homologous-recombination-proficient-cancers-to-parp-inhibition
#7
Lu Yang, Youyou Zhang, Weiwei Shan, Zhongyi Hu, Jiao Yuan, Jingjiang Pi, Yueying Wang, Lingling Fan, Zhaoqing Tang, Chunsheng Li, Xiaowen Hu, Janos L Tanyi, Yi Fan, Qihong Huang, Kathleen Montone, Chi V Dang, Lin Zhang
Strategies to enhance response to poly(adenosine diphosphate-ribose) polymerase inhibitor (PARPi) in primary and acquired homologous recombination (HR)-proficient tumors would be a major advance in cancer care. We used a drug synergy screen that combined a PARPi, olaparib, with 20 well-characterized epigenetic drugs and identified bromodomain and extraterminal domain inhibitors (BETis; JQ1, I-BET762, and OTX015) as drugs that acted synergistically with olaparib in HR-proficient cancer cells. Functional assays demonstrated that repressed BET activity reduces HR and thus enhances PARPi-induced DNA damage in cancer cells...
July 26, 2017: Science Translational Medicine
https://www.readbyqxmd.com/read/28746345/cisplatin-resistance-in-non-small-cell-lung-cancer-cells-is-associated-with-an-abrogation-of-cisplatin-induced-g2-m-cell-cycle-arrest
#8
Navin Sarin, Florian Engel, Ganna V Kalayda, Mareike Mannewitz, Jindrich Cinatl, Florian Rothweiler, Martin Michaelis, Hisham Saafan, Christoph A Ritter, Ulrich Jaehde, Roland Frötschl
The efficacy of cisplatin-based chemotherapy in cancer is limited by the occurrence of innate and acquired drug resistance. In order to better understand the mechanisms underlying acquired cisplatin resistance, we have compared the adenocarcinoma-derived non-small cell lung cancer (NSCLC) cell line A549 and its cisplatin-resistant sub-line A549rCDDP2000 with regard to cisplatin resistance mechanisms including cellular platinum accumulation, DNA-adduct formation, cell cycle alterations, apoptosis induction and activation of key players of DNA damage response...
2017: PloS One
https://www.readbyqxmd.com/read/28745237/anethole-inhibits-the-proliferation-of-human-prostate-cancer-cells-via-induction-of-cell-cycle-arrest-and-apoptosis
#9
Ayman Ibrahim Elkady
BACKGROUND: Prostate cancer-associated mortality is increasing at an alarming rate, which highlights the inevitability for unearthing novel agent for the management of this disease. Anethole, a major constituent of Foeniculum vulgare (fennel) essential oil, is widely used in folk medicine; it possesses anti-oxidant, anti-inflammatory, anti-proliferative and tumoricidal potentialities. OBJECTIVE: The current research was conducted to assess the impact of anethole on prostate cancer cell line, PC-3, and to delineate the molecular mechanism of action...
July 25, 2017: Anti-cancer Agents in Medicinal Chemistry
https://www.readbyqxmd.com/read/28744671/mechanisms-regulating-immune-surveillance-of-cellular-stress-in-cancer
#10
REVIEW
Ruth Seelige, Stephen Searles, Jack D Bui
The purpose of this review is to explore immune-mediated mechanisms of stress surveillance in cancer, with particular emphasis on the idea that all cancers have classical hallmarks (Hanahan and Weinberg in Cell 100:57-70, 67; Cell 144:646-674, 68) that could be interrelated. We postulate that hallmarks of cancer associated with cellular stress pathways (Luo et al. in Cell 136:823-837, 101) including oxidative stress, proteotoxic stress, mitotic stress, DNA damage, and metabolic stress could define and modulate the inflammatory component of cancer...
July 25, 2017: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/28743838/xpg-gene-rs751402-c-t-polymorphism-and-cancer-risk-evidence-from-22-publications
#11
Haixia Zhou, Ting-Yan Shi, Wenwen Zhang, Qiwen Li, Jinhong Zhu, Jing He, Jichen Ruan
The Xeroderma pigmentosum group G (XPG) gene promotes recognition and excision of damaged DNA during the DNA repair process. We conducted a comprehensive search of the MEDLINE, EMBASE, and Chinese Biomedical databases for publications evaluating the association XPG gene rs751402 C>T polymorphism and overall cancer risk. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were adopted to assess the strength of the association. A total of 22 publications encompassing 10538 cases and 10511 control subjects were included in the final meta-analysis...
July 18, 2017: Oncotarget
https://www.readbyqxmd.com/read/28741503/the-pushmi-pullyu-of-dna-repair-clinical-synthetic-lethality
#12
REVIEW
S Percy Ivy, Johann de Bono, Elise C Kohn
Maintenance of genomic integrity is critical for adaptive survival in the face of endogenous and exogenous environmental stress. The loss of stability and fidelity in the genome caused by cancer and cancer treatment provides therapeutic opportunities to leverage the critical balance between DNA injury and repair. Blocking repair and pushing damaged DNA through the cell cycle using therapeutic inhibitors exemplify the 'pushmi-pullyu' effect of disrupted DNA repair. DNA repair inhibitors (DNARi) can be separated into five biofunctional categories: sensors, mediators, transducers, effectors, and collaborators that recognize DNA damage, propagate injury DNA messages, regulate cell cycle checkpoints, and alter the microenvironment...
November 2016: Trends in Cancer
https://www.readbyqxmd.com/read/28740569/dna-oncogenic-virus-induced-oxidative-stress-genomic-damage-and-aberrant-epigenetic-alterations
#13
REVIEW
Mankgopo Magdeline Kgatle, Catherine Wendy Spearman, Asgar Ali Kalla, Henry Norman Hairwadzi
Approximately 20% of human cancers is attributable to DNA oncogenic viruses such as human papillomavirus (HPV), hepatitis B virus (HBV), and Epstein-Barr virus (EBV). Unrepaired DNA damage is the most common and overlapping feature of these DNA oncogenic viruses and a source of genomic instability and tumour development. Sustained DNA damage results from unceasing production of reactive oxygen species and activation of inflammasome cascades that trigger genomic changes and increased propensity of epigenetic alterations...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28740404/reactive-oxygen-species-mediate-soft-corals-derived-sinuleptolide-induced-antiproliferation-and-dna-damage-in-oral-cancer-cells
#14
Yung-Ting Chang, Chiung-Yao Huang, Jen-Yang Tang, Chih-Chuang Liaw, Ruei-Nian Li, Jing-Ru Liu, Jyh-Horng Sheu, Hsueh-Wei Chang
We previously reported that the soft coral-derived bioactive substance, sinuleptolide, can inhibit the proliferation of oral cancer cells in association with oxidative stress. The functional role of oxidative stress in the cell-killing effect of sinuleptolide on oral cancer cells was not investigated as yet. To address this question, we introduced the reactive oxygen species (ROS) scavenger (N-acetylcysteine [NAC]) in a pretreatment to evaluate the sinuleptolide-induced changes to cell viability, morphology, intracellular ROS, mitochondrial superoxide, apoptosis, and DNA damage of oral cancer cells (Ca9-22)...
2017: OncoTargets and Therapy
https://www.readbyqxmd.com/read/28739395/sterigmatocystin-induced-apoptosis-in-human-pulmonary-cells-in-vitro
#15
Jinfeng Cui, Juan Wang, Shujuan Huang, Xiujuan Jiang, Yuehong Li, Wenxin Wu, Xianghong Zhang
Sterigmatocystin (ST) is generally recognized as a potential carcinogen, mutagen and teratogen. Studies showed that ST could induce adenocarcinoma of lung in mice in vivo and DNA damage, cell cycle arrest in a human immortalized bronchial epithelial cell line (BEAS-2B cells) and a human lung cancer cell line (A549 cells) in vitro. Besides, ST could induce G2 arrest (cell cycle arrest in G2 phase) in several other cells. Cell cycle arrest may be one of the common toxic effects of ST. As cells may undergo apoptosis or death due to cell cycle arrest, we wondered whether apoptosis is another common effect of ST in different cells in vitro...
July 21, 2017: Experimental and Toxicologic Pathology: Official Journal of the Gesellschaft Für Toxikologische Pathologie
https://www.readbyqxmd.com/read/28739375/oxidative-stress-and-inhibition-of-nitric-oxide-generation-underlie-methotrexate-induced-senescence-in-human-colon-cancer-cells
#16
Magdalena Dabrowska, Lukasz Uram, Zbigniew Zielinski, Wojciech Rode, Ewa Sikora
The response of human colon cancer C85 cells to methotrexate takes the form of reversible growth arrest of the type of stress-induced senescence. In the present study it is shown that during C85 cell progression into methotrexate-induced senescence, dihydrofolate reductase, the primary intracellular target for the drug, is stabilized at the protein level and its enzymatic activity, assayed in crude cellular extracts, decreases by 2-fold. Dihydrofolate reductase inhibition results in an increase in dihydrobiopterin level and an ultimate decrease in the tetrahydrobiopterin: dihydrobiopterin ratio in senescent cells...
July 21, 2017: Mechanisms of Ageing and Development
https://www.readbyqxmd.com/read/28738860/germline-emsy-sequence-alterations-in-hereditary-breast-cancer-and-ovarian-cancer-families
#17
Kirsi M Määttä, Riikka Nurminen, Minna Kankuri-Tammilehto, Anne Kallioniemi, Satu-Leena Laasanen, Johanna Schleutker
BACKGROUND: BRCA1 and BRCA2 mutations explain approximately one-fifth of the inherited susceptibility in high-risk Finnish hereditary breast and ovarian cancer (HBOC) families. EMSY is located in the breast cancer-associated chromosomal region 11q13. The EMSY gene encodes a BRCA2-interacting protein that has been implicated in DNA damage repair and genomic instability. We analysed the role of germline EMSY variation in breast/ovarian cancer predisposition. The present study describes the first EMSY screening in patients with high familial risk for this disease...
July 24, 2017: BMC Cancer
https://www.readbyqxmd.com/read/28738540/regulatory-players-of-dna-damage-repair-mechanisms-role-in-cancer-chemoresistance
#18
REVIEW
Kunnathur Murugesan Sakthivel, Sreedharan Hariharan
DNA damaging agents are most common in chemotherapeutic molecules that act against cancer. However, cancer cells possess inherent biological features to overcome DNA damages by activating various distinct repair mechanisms and pathways. Importantly, various oncogenes, cancer stem cells (CSCs), hypoxic environment, transcription factors and bystander signaling that are activated in the cancer cells influence DNA repair, thereby effectively repairing the DNA damage. Repaired cancer cells often become more resistance to further therapy and results in disease recurrence...
July 20, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28738408/cgas-surveillance-of-micronuclei-links-genome-instability-to-innate-immunity
#19
Karen J Mackenzie, Paula Carroll, Carol-Anne Martin, Olga Murina, Adeline Fluteau, Daniel J Simpson, Nelly Olova, Hannah Sutcliffe, Jacqueline K Rainger, Andrea Leitch, Ruby T Osborn, Ann P Wheeler, Marcin Nowotny, Nick Gilbert, Tamir Chandra, Martin A M Reijns, Andrew P Jackson
DNA is strictly compartmentalized within the nucleus to prevent autoimmunity; despite this, cyclic GMP-AMP synthase (cGAS), a cytosolic sensor of double-stranded DNA, is activated in autoinflammatory disorders and by DNA damage. Precisely how cellular DNA gains access to the cytoplasm remains to be determined. Here, we report that cGAS localizes to micronuclei arising from genome instability in a mouse model of monogenic autoinflammation, after exogenous DNA damage and spontaneously in human cancer cells. Such micronuclei occur after mis-segregation of DNA during cell division and consist of chromatin surrounded by its own nuclear membrane...
July 24, 2017: Nature
https://www.readbyqxmd.com/read/28737827/cytotoxic-and-chemosensitization-effects-of-scutellarin-from-traditional-chinese-herb-scutellaria%C3%A2-altissima%C3%A2-l-in-human-prostate-cancer-cells
#20
Chen Gao, Yinglu Zhou, Zhongling Jiang, Yuan Zhao, Dongjun Zhang, Xia Cong, Rongfeng Cao, Huatao Li, Wenru Tian
Scutellaria altissima L. is a common traditional Chinese medicine used to treat inflammation in some countries. Scutellarin, an active major flavone glycoside isolated from the traditional Chinese medicine Scutellaria altissima L., has been shown to offer various beneficial biochemical effects on cerebrovascular diseases and inflammation. However, the antiproliferative effects of Scutellarin in prostate cancer and the underlying mechanism are not fully elucidated. In the present study, we aimed to ascertain whether Scutellarin inhibits cancer cell growth and to further explore the molecular mechanism...
July 24, 2017: Oncology Reports
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