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https://www.readbyqxmd.com/read/27887917/microrna-136-inhibits-cancer-stem-cell-activity-and-enhances-the-anti-tumor-effect-of-paclitaxel-against-chemoresistant-ovarian-cancer-cells-by-targeting-notch3
#1
Ju-Yeon Jeong, Hae-Youn Kang, Tae-Heon Kim, Gwang-Il Kim, Jin-Hyung Huh, Ah-Young Kwon, Se-Wha Kim, Sang-Geun Jung, Hee-Jung An
To identify microRNAs (miRNAs) regulating Notch3 expression in association with paclitaxel resistance, candidate miRNAs targeting Notch3 were predicted using TargetScan. We found that miR-136 directly targets Notch3, and miR-136 was significantly downregulated in OSC tissues relative to normal control tissues, and low expression of miR-136 correlated with poor overall in ovarian cancer patients. Artificial miR-136 overexpression significantly reduced cell viability, proliferation, CSC spheroid formation, and angiogenesis, and increased apoptosis in paclitaxel-resistant SKpac cells compared with the effects of paclitaxel alone...
November 22, 2016: Cancer Letters
https://www.readbyqxmd.com/read/27875301/an-intrinsically-disordered-aplf-links-ku-dna-pkcs-and-xrcc4-dna-ligase-iv-in-an-extended-flexible-non-homologous-end-joining-complex
#2
Michal Hammel, Yaping Yu, Sarvan Kumar Radhakrishnan, Chirayu Chokshi, Miaw-Sheue Tsai, Yoshihiro Matsumoto, Monica Kuzdovich, Soumya G Remesh, Shujuan Fang, Alan E Tomkinson, Susan P Lees-Miller, John A Tainer
DNA double-strand break (DSB) repair by non-homologous end joining (NHEJ) in human cells is initiated by Ku heterodimer binding to a DSB, followed by recruitment of core NHEJ factors including DNA-dependent protein kinase catalytic subunit (DNA-PKcs), XRCC4-like factor (XLF) and XRCC4 (X4)-DNA ligase IV (L4). In addition, Ku interacts with accessory factors such as Aprataxin and Polynucleotide kinase/phosphatase-Like Factor (APLF), yet how these factors interact to tether, process and ligate DSB ends while allowing regulation and chromatin interactions remains enigmatic...
November 14, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27829214/pict-1-is-a-key-nucleolar-sensor-in-dna-damage-response-signaling-that-regulates-apoptosis-through-the-rpl11-mdm2-p53-pathway
#3
Hongbo Chen, Liqiao Han, Hsiangi Tsai, Zhiwei Wang, Yanping Wu, Yanhong Duo, Wei Cao, Lijun Chen, Zhirong Tan, Ning Xu, Xianzhang Huang, Junhua Zhuang, Laiqiang Huang
PICT-1 is an essential ribosome biogenesis factor whose loss induces p53 accumulation and apoptosis. Here, we show that DNA damage changes PICT-1 localization and decreases PICT-1 protein levels via the proteasome pathway. Two important phosphatidylinositol 3-kinase-like kinases (PIKKs), ataxia-telangiectasia mutated (ATM) and the Ku70 subunit of DNA-dependent protein kinase (DNA-PK), co-localize and interact with PICT-1 in the nucleolus. Computational prediction of phosphorylation sites and detection using an anti-phospho-substrate antibody suggest that PICT-1 might be a substrate of PIKKs...
November 4, 2016: Oncotarget
https://www.readbyqxmd.com/read/27813122/quercetin-alters-the-dna-damage-response-in-human-hematopoietic-stem-and-progenitor-cells-via-topoii-and-pi3k-dependent-mechanisms-synergizing-in-leukemogenic-rearrangements
#4
Shahar Biechonski, Dana Gourevich, Melanie Rall, Nasma Aqaqe, Muhammad Yassin, Adi Zipin-Roitman, Luba Trakhtenbrot, Leonid Olender, Yael Raz, Ariel J Jaffa, Dan Grisaru, Lisa Wiesmuller, David Elad, Michael Milyavsky
Quercetin (Que) is an abundant flavonoid in the human diet and high-concentration food supplement with reported pro- and anti- carcinogenic activities. Topoisomerase II (TopoII) inhibition and subsequent DNA damage induction by Que was implicated in the Mixed Lineage Leukemia gene (MLL) rearrangements that can induce infant and adult leukemias. This notion raised concerns regarding possible genotoxicities of Que in Hematopoietic Stem and Progenitor Cells (HSPCs). However, molecular targets mediating Que effects on DNA repair relevant to MLL translocations have not been defined...
November 3, 2016: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/27776457/homologous-recombination-preferentially-repairs-heat-induced-dna-double-strand-breaks-in-mammalian-cells
#5
Akihisa Takahashi, Eiichiro Mori, Yosuke Nakagawa, Atsuhisa Kajihara, Tadaaki Kirita, L Pittman Douglas, Masatoshi Hasegawa, Takeo Ohnishi
PURPOSE: Heat shock induces DNA double-strand breaks (DSBs), but the precise mechanism of repairing heat-induced damage is unclear. Here, we investigated the DNA repair pathways involved in cell death induced by heat shock. MATERIALS AND METHODS: B02, a specific inhibitor of human RAD51 (homologous recombination; HR), and NU7026, a specific inhibitor of DNA-PK (non-homologous end-joining; NHEJ), were used for survival assays of human cancer cell lines with different p53-gene status...
October 24, 2016: International Journal of Hyperthermia
https://www.readbyqxmd.com/read/27765510/synthesis-of-linear-and-angular-aryl-morpholino-naphth-oxazines-their-dna-pk-pi3k-pde3a-and-antiplatelet-activity
#6
Rick Morrison, Zhaohua Zheng, Ian G Jennings, Philip E Thompson, Jasim M A Al-Rawi
To continue our study of 2-morpholino-benzoxazine based compounds, which show useful activity against PI3K family enzymes or antiplatelet activity, we designed and synthesized a series of linear 6.7-fused, 5,6-angular fused and 7,8-angular fused-aryl-morpholino-naphth-oxazines. The compounds were prepared from substituted 2-hydroxynaphthoic acid to give the corresponding thioxo analogues 8, 9, 15 and 19. The thioxo products were then converted to the morpholino substituted analogue. The aryl group was introduced by Suzuki coupling of bromo precursors...
October 5, 2016: Bioorganic & Medicinal Chemistry Letters
https://www.readbyqxmd.com/read/27764514/sirtuins-and-their-interactions-with-transcription-factors-and-poly-adp-ribose-polymerases
#7
H Jęśko, R P Strosznajder
Sirtuins (SIRT1 to -7) are unique histone deacetylases (HDACs) whose activity depends on NAD+, thus making them capable of sensing the cellular metabolic status. Sirtuins orchestrate the stress response and damage repair, and are able to modulate the course of ageing and neurodegenerative diseases. Despite their classification as HDACs, sirtuins deacetylate a vast number of targets in many cellular compartments, and some display additional enzymatic activities including mono(ADP-ribosyl)ation. SIRTs interact with multiple signalling proteins, transcription factors and enzymes including p53, FOXOs (forkhead box subgroup O), PPARs (peroxisome proliferator-activated receptors), NF-B, and DNA-PK (DNA-dependent protein kinase)...
2016: Folia Neuropathologica
https://www.readbyqxmd.com/read/27723831/the-architectural-chromatin-factor-high-mobility-group-a1-enhances-dna-ligase-iv-activity-influencing-dna-repair
#8
Ilenia Pellarin, Laura Arnoldo, Silvia Costantini, Silvia Pegoraro, Gloria Ros, Carlotta Penzo, Gianluca Triolo, Francesca Demarchi, Riccardo Sgarra, Alessandro Vindigni, Guidalberto Manfioletti
The HMGA1 architectural transcription factor is an oncogene overexpressed in the vast majority of human cancers. HMGA1 is a highly connected node in the nuclear molecular network and the key aspect of HMGA1 involvement in cancer development is that HMGA1 simultaneously confers cells multiple oncogenic hits, ranging from global chromatin structural and gene expression modifications up to the direct functional alterations of key cellular proteins. Interestingly, HMGA1 also modulates DNA damage repair pathways...
2016: PloS One
https://www.readbyqxmd.com/read/27702817/ovarian-cancers-harbour-defects-in-non-homologous-end-joining-resulting-in-resistance-to-rucaparib
#9
Aiste McCormick, Peter Donoghue, Michelle Dixon, Richard O'Sullivan, Rachel Louise O'Donnell, James Murray, Angelika Kaufmann, Nicola J Curtin, Richard J Edmondson
PURPOSE: DNA damage defects are common in ovarian cancer and can be used to stratify treatment. Although most work has focussed on Homologous Recombination (HR), DNA double strand breaks are repaired primarily by non-homologous end joining (NHEJ). Defects in NHEJ have been shown to contribute to genomic instability and have been associated with the development of chemoresistance. EXPERIMENTAL DESIGN: NHEJ was assessed in a panel of ovarian cancer cell lines and 47 primary ascitic derived ovarian cancer cultures, by measuring the ability of cell extracts to end-join linearized plasmid monomers into multimers...
October 4, 2016: Clinical Cancer Research: An Official Journal of the American Association for Cancer Research
https://www.readbyqxmd.com/read/27693461/inhibition-of-atr-dependent-feedback-activation-of-chk1-sensitises-cancer-cells-to-chk1-inhibitor-monotherapy
#10
Andrew J Massey
The Chk1 and ATR kinases are critical mediators of the DNA damage response pathway and help protect cancer cells from endogenous and oncogene induced replication stress. Inhibitors of both kinases are currently being evaluated in clinical trials. Chk1 inhibition with V158411 increases DNA damage and activates the ATR, ATM and DNA-PKcs dependent DNA damage response pathways. Inhibiting ATR, ATM and/or DNA-PKcs has the potential to increase the therapeutic activity of Chk1 inhibitors. ATR inhibition but not ATM or DNA-PKcs inhibition potentiated the cytotoxicity of V158411 in p53 mutant and wild type human cancer cell lines...
September 28, 2016: Cancer Letters
https://www.readbyqxmd.com/read/27690730/chk1-and-dna-pk-mediate-tpen-induced-dna-damage-in-a-ros-dependent-manner-in-human-colon-cancer-cells
#11
Omar Nasser Rahal, Maamoun Fatfat, Carla Hankache, Bassam Osman, Hala Khalife, Khaled Machaca, Hala-Gali Muhtasib
Recently, we showed that the metal chelator TPEN targets colon cancer cells through redox cycling of copper. Here, we studied the DNA damage potential of TPEN and deciphered the role of Chk1, ATM and DNA-PK in TPEN-induced toxicity in 3 human colon cancer cell lines, HCT116, SW480 and HT29. We also investigated the role of reactive oxygen species (ROS) in TPEN-induced DNA damage. TPEN reduced cell viability in a dose- and time-dependent manner. Cytotoxicity was associated with significant DNA damage and higher expression of γ-H2AX protein and activation of ATM/ATR signaling pathway...
October 3, 2016: Cancer Biology & Therapy
https://www.readbyqxmd.com/read/27675958/rnf8-regulates-nonhomologous-end-joining-and-dna-pk-recruitment-to-dna-double-strand-break-sites
#12
S Gao, Y Surovtseva, R S Bindra
No abstract text is available yet for this article.
October 1, 2016: International Journal of Radiation Oncology, Biology, Physics
https://www.readbyqxmd.com/read/27668603/-role-of-dna-dependent-protein-kinase-in-the-hiv-1-replication-cycle
#13
E S Knyazhanskaya, O A Shadrina, A N Anisenko, M B Gottikh
Human immunodeficiency virus type 1 (HIV-1) is among the best-studied viruses, but some aspects of HIV-1 biology remain obscure. The role of cell proteins in virus replication raises especially many questions. One of the proteins is DNA-dependent protein kinase (DNA-PK), which performs crucially important functions in the human body. DNA-PK is known to influence at least two stages in the HIV-1 life cycle, the integration of viral genome in cell DNA and transcription of the integrated provirus. Many details regarding this influence remain unresolved...
July 2016: Molekuliarnaia Biologiia
https://www.readbyqxmd.com/read/27643582/comparison-of-the-radiosensitizing-effect-of-atr-atm-and-dna-pk-kinase-inhibitors-on-cervical-carcinoma-cells
#14
J Vávrová, L Zárybnická, P Jošt, A Tichý, M Řezáčová, Z Šinkorová, J Pejchal
Here, we compared the effects of inhibitors of three phosphatidylinositol-3-kinase-related kinases, ATM, ATR a DNA-PK, on radiosensitization of cervical carcinoma cells. We demonstrated that DNA-PK inhibitor NU7441 enhanced phosphorylation of Chk1 and Chk2 kinases 2 h after irradiation of HeLa cells at a dose of 8 Gy in contrast to ATM kinase inhibitor KU55933, which completely blocked the Chk2 kinase phosphorylation on threonine 68, and ATR kinase inhibitor VE-821, which blocked the Chk1 kinase phosphorylation on serine 345...
2016: Folia Biologica (Praha)
https://www.readbyqxmd.com/read/27621574/perspectives-on-the-combination-of-radiotherapy-and-targeted-therapy-with-dna-repair-inhibitors-in-the-treatment-of-pancreatic-cancer
#15
REVIEW
Shih-Hung Yang, Ting-Chun Kuo, Hsu Wu, Jhe-Cyuan Guo, Chiun Hsu, Chih-Hung Hsu, Yu-Wen Tien, Kun-Huei Yeh, Ann-Lii Cheng, Sung-Hsin Kuo
Pancreatic cancer is highly lethal. Current research that combines radiation with targeted therapy may dramatically improve prognosis. Cancerous cells are characterized by unstable genomes and activation of DNA repair pathways, which are indicated by increased phosphorylation of numerous factors, including H2AX, ATM, ATR, Chk1, Chk2, DNA-PKcs, Rad51, and Ku70/Ku80 heterodimers. Radiotherapy causes DNA damage. Cancer cells can be made more sensitive to the effects of radiation (radiosensitization) through inhibition of DNA repair pathways...
August 28, 2016: World Journal of Gastroenterology: WJG
https://www.readbyqxmd.com/read/27599846/dna-damage-response-curtails-detrimental-replication-stress-and-chromosomal-instability-induced-by-the-dietary-carcinogen-phip
#16
Maximilian Mimmler, Simon Peter, Alexander Kraus, Svenja Stroh, Teodora Nikolova, Nina Seiwert, Solveig Hasselwander, Carina Neitzel, Jessica Haub, Bernhard H Monien, Petra Nicken, Pablo Steinberg, Jerry W Shay, Bernd Kaina, Jörg Fahrer
PhIP is an abundant heterocyclic aromatic amine (HCA) and important dietary carcinogen. Following metabolic activation, PhIP causes bulky DNA lesions at the C8-position of guanine. Although C8-PhIP-dG adducts are mutagenic, their interference with the DNA replication machinery and the elicited DNA damage response (DDR) have not yet been studied. Here, we analyzed PhIP-triggered replicative stress and elucidated the role of the apical DDR kinases ATR, ATM and DNA-PKcs in the cellular defense response. First, we demonstrate that PhIP induced C8-PhIP-dG adducts and DNA strand breaks...
December 1, 2016: Nucleic Acids Research
https://www.readbyqxmd.com/read/27593924/cd133-and-dna-pk-regulate-mdr1-via-the-pi3k-or-akt-nf-%C3%AE%C2%BAb-pathway-in-multidrug-resistant-glioblastoma-cells-in-vitro
#17
G Xi, E Hayes, R Lewis, S Ichi, B Mania-Farnell, K Shim, T Takao, E Allender, C S Mayanil, T Tomita
No abstract text is available yet for this article.
September 5, 2016: Oncogene
https://www.readbyqxmd.com/read/27572101/casticin-induces-dna-damage-and-inhibits-dna-repair-associated-protein-expression-in-b16f10-mouse-melanoma-cancer-cells
#18
Yung-Luen Shih, Jason Chou, Ming-Yang Yeh, Hsiao-Min Chou, Hsiu-Chen Chou, Hsu-Feng Lu, Hung-Sheng Shang, Fu-Shin Chueh, Yung-Lin Chu, Shu-Ching Hsueh, Jing-Gung Chung
Casticin, a polymethoxyflavone, has been demonstrated to possess anticancer activities, yet no study has shown in detail that casticin induces DNA damage in lung cancer cells. The purpose of this study was to investigate the possible molecular mechanisms of casticin which induce DNA damage and nuclear condensation in murine melanoma cancer B16F10 cells. In this study, by examining and capturing images using phase contrast microscopy, we found that casticin induced cell morphological changes. Moreover, it decreased the total number of viable cells which was measured by flow cytometry...
October 2016: Oncology Reports
https://www.readbyqxmd.com/read/27566146/sox9-is-targeted-for-proteasomal-degradation-by-the-e3-ligase-fbw7-in-response-to-dna-damage
#19
Xuehui Hong, Wenyu Liu, Ruipeng Song, Jamie J Shah, Xing Feng, Chi Kwan Tsang, Katherine M Morgan, Samuel F Bunting, Hiroyuki Inuzuka, X F Steven Zheng, Zhiyuan Shen, Hatem E Sabaawy, LianXin Liu, Sharon R Pine
SOX9 encodes a transcription factor that governs cell fate specification throughout development and tissue homeostasis. Elevated SOX9 is implicated in the genesis and progression of human tumors by increasing cell proliferation and epithelial-mesenchymal transition. We found that in response to UV irradiation or genotoxic chemotherapeutics, SOX9 is actively degraded in various cancer types and in normal epithelial cells, through a pathway independent of p53, ATM, ATR and DNA-PK. SOX9 is phosphorylated by GSK3β, facilitating the binding of SOX9 to the F-box protein FBW7α, an E3 ligase that functions in the DNA damage response pathway...
October 14, 2016: Nucleic Acids Research
https://www.readbyqxmd.com/read/27550181/multipronged-regulatory-functions-of-a-novel-endonuclease-tiea-from-helicobacter-pylori
#20
Savita Devi, Suhail A Ansari, Shivendra Tenguria, Naveen Kumar, Niyaz Ahmed
Helicobacter pylori portrays a classical paradigm of persistent bacterial infections. A well balanced homeostasis of bacterial effector functions and host responses is purported to be the key in achieving long term colonization in specific hosts. H. pylori nucleases have been shown to assist in natural transformation, but their role in virulence and colonization remains elusive. Therefore, it is imperative to understand the involvement of these nucleases in the pathogenesis of H. pylori Here, we report the multifaceted role of a TNFR-1 interacting endonuclease A (TieA) from H...
August 22, 2016: Nucleic Acids Research
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