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https://www.readbyqxmd.com/read/28938460/huwe1-regulates-the-establishment-and-maintenance-of-spermatogonia-by-suppressing-dna-damage-response
#1
Kin Lam Fok, Rohini Bose, Kai Sheng, Ching-Wen Chang, Mira Katz-Egorov, Martine Culty, Sicheng Su, Ming Yang, Ye Chun Ruan, Hsiao-Chang Chan, Antonio Iavarone, Anna Lasorella, Regina Cencic, Jerry Pelletier, Makoto Nagano, Wenming Xu, Simon S Wing
Spermatogenesis is sustained by a heterogeneous population of spermatogonia which includes the spermatogonial stem cells. However, the mechanisms underlying their establishment from gonocyte embryonic precursors and their maintenance thereafter remain largely unknown. Here, we report that inactivation of the ubiquitin ligase Huwe1 in male germ cells in mice led to the degeneration of spermatogonia in neonates and resulted in a Sertoli cell-only phenotype in the adult. Huwe1 KO gonocytes showed a decrease in mitotic re-entry which inhibited their transition to spermatogonia...
August 25, 2017: Endocrinology
https://www.readbyqxmd.com/read/28937650/explaining-the-microtubule-energy-balance-contributions-due-to-dipole-moments-charges-van-der-waals-and-solvation-energy
#2
Ahmed Taha Ayoub, Michael Staelens, Alessio Prunotto, Marco A Deriu, Andrea Danani, Mariusz Klobukowski, Jack Adam Tuszynski
Microtubules are the main components of mitotic spindles, and are the pillars of the cellular cytoskeleton. They perform most of their cellular functions by virtue of their unique dynamic instability processes which alternate between polymerization and depolymerization phases. This in turn is driven by a precise balance between attraction and repulsion forces between the constituents of microtubules (MTs)-tubulin dimers. Therefore, it is critically important to know what contributions result in a balance of the interaction energy among tubulin dimers that make up microtubules and what interactions may tip this balance toward or away from a stable polymerized state of tubulin...
September 22, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28935673/publisher-s-note-chromosomal-breaks-during-mitotic-catastrophe-trigger-%C3%AE-h2ax-atm-p53-mediated-apoptosis-gabriela-imreh-helin-vakifahmetoglu-norberg-stefan-imreh-boris-zhivotovsky-j-cell-sci-doi-10-1242-jcs-081612
#3
https://www.readbyqxmd.com/read/28928827/inhibition-of-c-myc-expression-accounts-for-an-increase-in-the-number-of-multinucleated-cells-in-human-cervical-epithelial-cells
#4
Feng Mei Cui, Xiu Jin Sun, Cheng Cheng Huang, Qiu Chen, Yong Ming He, Shi Meng Zhang, Hua Guan, Man Song, Ping Kun Zhou, Jun Hou
The present study aimed to explore the mechanisms by which c-Myc is involved in mitotic catastrophe. HeLa-630 is a cell line stably silenced for c-Myc expression that was established in the laboratory of the School of Radiation Medicine and Protection. Multinucleated cells were observed in this line, and gene expression analysis was utilized to examine differences in gene expression in these cells compared with in the control cells transfected with the control plasmid. Gene ontology analysis was performed for differentially expressed genes...
September 2017: Oncology Letters
https://www.readbyqxmd.com/read/28927115/wee1-inhibition-by-mk1775-as-a-single-agent-therapy-inhibits-ovarian-cancer-viability
#5
Minghui Zhang, Donye Dominguez, Siqi Chen, Jie Fan, Lei Qin, Alan Long, Xia Li, Yi Zhang, Huirong Shi, Bin Zhang
Wee1-like protein kinase (WEE1) physiologically serves a key function in maintaining the integrity of the cell genome through mediating the activation of cyclin-dependent kinase (CDK)1 and CDK2. Increased expression of WEE1 has been associated with the poor prognosis of patients with ovarian cancer. The present study aimed at examining the in vitro and in vivo antitumor activity of MK1775, a potent pharmacological inhibitor of WEE1, as a single agent against ovarian cancer cells. The cytotoxicity of MK1775 was examined in a panel of tumor cells using MTT in vitro...
September 2017: Oncology Letters
https://www.readbyqxmd.com/read/28925395/small-molecules-targeted-to-the-microtubule-hec1-interaction-inhibit-cancer-cell-growth-through-microtubule-stabilization
#6
M Ferrara, G Sessa, M Fiore, F Bernard, I A Asteriti, E Cundari, G Colotti, S Ferla, M Desideri, S Buglioni, D Trisciuoglio, D Del Bufalo, A Brancale, F Degrassi
Highly expressed in cancer protein 1 (Hec1) is a subunit of the kinetochore (KT)-associated Ndc80 complex, which ensures proper segregation of sister chromatids at mitosis by mediating the interaction between KTs and microtubules (MTs). HEC1 mRNA and protein are highly expressed in many malignancies as part of a signature of chromosome instability. These properties render Hec1 a promising molecular target for developing therapeutic drugs that exert their anticancer activities by producing massive chromosome aneuploidy...
September 18, 2017: Oncogene
https://www.readbyqxmd.com/read/28916678/gucy2c-signaling-opposes-the-acute-radiation-induced-gi-syndrome
#7
Peng Li, Evan Wuthrick, Jeff A Rappaport, Crystal Kraft, Jieru E Lin, Glen Marszalowicz, Adam E Snook, Tingting Zhan, Terry M Hyslop, Scott A Waldman
High doses of ionizing radiation induce acute damage to epithelial cells of the gastrointestinal (GI) tract, mediating toxicities restricting the therapeutic efficacy of radiation in cancer and morbidity and mortality in nuclear disasters. No approved prophylaxis or therapy exists for these toxicities, in part reflecting an incomplete understanding of mechanisms contributing to the acute radiation-induced GI syndrome (RIGS). Guanylate cyclase C (GUCY2C) and its hormones guanylin and uroguanylin have recently emerged as one paracrine axis defending intestinal mucosal integrity against mutational, chemical, and inflammatory injury...
September 15, 2017: Cancer Research
https://www.readbyqxmd.com/read/28852020/co-delivery-of-paclitaxel-and-cetuximab-by-nanodiamond-enhances-mitotic-catastrophe-and-tumor-inhibition
#8
Yu-Wei Lin, Emmanuel Naveen Raj, Wei-Siang Liao, Johnson Lin, Kuang-Kai Liu, Ting-Hua Chen, Hsiao-Chun Cheng, Chi-Ching Wang, Lily Yi Li, Chinpiao Chen, Jui-I Chao
The poor intracellular uptake and non-specific binding of anticancer drugs into cancer cells are the bottlenecks in cancer therapy. Nanocarrier platforms provide the opportunities to improve the drug efficacy. Here we show a carbon-based nanomaterial nanodiamond (ND) that carried paclitaxel (PTX), a microtubule inhibitor, and cetuximab (Cet), a specific monoclonal antibody against epidermal growth factor receptor (EGFR), inducing mitotic catastrophe and tumor inhibition in human colorectal cancer (CRC). ND-PTX blocked the mitotic progression, chromosomal separation, and induced apoptosis in the CRC cells; however, NDs did not induce these effects...
August 29, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28839115/genome-scale-genetic-interactions-and-cell-imaging-confirm-cytokinesis-as-deleterious-to-transient-topoisomerase-ii-deficiency-in-saccharomyces-cerevisiae
#9
Cristina Ramos-Pérez, Jessel Ayra-Plasencia, Emiliano Matos-Perdomo, Michael Lisby, Grant W Brown, Félix Machín
Topoisomerase II (Top2) is the essential protein that resolves DNA catenations. When Top2 is inactivated, mitotic catastrophe results from massive entanglement of chromosomes. Top2 is also the target of many first-line anticancer drugs, the so-called Top2 poisons. Often, tumors become resistant to these drugs by acquiring hypomorphic mutations in the genes encoding Top2. Here, we have compared the cell cycle and nuclear segregation of two coisogenic Saccharomyces cerevisiae strains carrying top2 thermosensitive alleles that differ in their resistance to Top2 poisons: the broadly-used poison-sensitive top2-4 and the poison-resistant top2-5 Furthermore, we have performed genome-scale Synthetic Genetic Array (SGA) analyses for both alleles under permissive conditions, chronic sublethal Top2 downregulation and acute, yet transient, Top2 inactivation...
August 24, 2017: G3: Genes—Genomes—Genetics
https://www.readbyqxmd.com/read/28830982/targeting-tao-kinases-using-a-new-inhibitor-compound-delays-mitosis-and-induces-mitotic-cell-death-in-centrosome-amplified-breast-cancer-cells
#10
Chuay-Yeng Koo, Caterina Giacomini, Marta Reyes-Corral, Yolanda Olmos, Ignatius A Tavares, Charles M Marson, Spiros Linardopoulos, Andrew N Tutt, Jonathan D H Morris
Thousand-and-one amino acid kinases (TAOKs) 1 and 2 are activated catalytically during mitosis and can contribute to mitotic cell rounding and spindle positioning. Here, we characterize a compound that inhibits TAOK1 and TAOK2 activity with IC50 values of 11-15 nM, is ATP-competitive and targets these kinases selectively. TAOK inhibition or depletion in centrosome amplified SKBR3 or BT549 breast cancer cell models increases the mitotic population, the percentages of mitotic cells displaying amplified centrosomes and multipolar spindles, induces cell death and inhibits cell growth...
August 22, 2017: Molecular Cancer Therapeutics
https://www.readbyqxmd.com/read/28807940/mitotic-vulnerability-in-triple-negative-breast-cancer-associated-with-lin9-is-targetable-with-bet-inhibitors
#11
Jennifer M Sahni, Sylvia S Gayle, Bryan Webb, Kristen L Weber-Bonk, Darcie D Seachrist, Salendra Singh, Steven T Sizemore, Nicole A Restrepo, Gurkan Bebek, Peter Scacheri, Vinay Varadan, Matthew K Summers, Ruth A Keri
Triple-negative breast cancers (TNBC) are highly aggressive, lack FDA-approved targeted therapies, and frequently recur, making the discovery of novel therapeutic targets for this disease imperative. Our previous analysis of the molecular mechanisms of action of Bromodomain and extraterminal protein inhibitors (BETi) in TNBC revealed these drugs cause multinucleation, indicating BET proteins are essential for efficient mitosis and cytokinesis. Here, using live cell imaging, we show that BET inhibition prolonged mitotic progression and induced mitotic cell death, both of which are indicative of mitotic catastrophe...
August 14, 2017: Cancer Research
https://www.readbyqxmd.com/read/28767448/selective-cytotoxicity-of-vanadium-complexes-on-human-pancreatic-ductal-adenocarcinoma-cell-line-by-inducing-necroptosis-apoptosis-and-mitotic-catastrophe-process
#12
Szymon Kowalski, Stanisław Hać, Dariusz Wyrzykowski, Agata Zauszkiewicz-Pawlak, Iwona Inkielewicz-Stępniak
The pancreatic cancer is the fourth leading cause of cancer-related death and characterized by one of the lowest five-year survival rate. The current therapeutic options are demonstrating minimal effectiveness, therefore studies on new potential anticancer compounds, with non-significant side effects are highly desirable. Recently, it was demonstrated that vanadium compounds, in particular organic derivatives, exhibit anticancer properties against different type of tumor as well as favorable biodistribution from a pancreatic cancer treatment perspective...
July 22, 2017: Oncotarget
https://www.readbyqxmd.com/read/28759878/thienopyrimidine-derivatives-exert-their-anticancer-efficacy-via-apoptosis-induction-oxidative-stress-and-mitotic-catastrophe
#13
Haneen Amawi, Chandrabose Karthikeyan, Rekha Pathak, Noor Hussein, Ryann Christman, Robert Robey, Charles R Ashby, Piyush Trivedi, Ashim Malhotra, Amit K Tiwari
In this study, a series of 13 structural variants of thieno[2,3d]pyrimidine derivatives (6a-6m) were synthesized and screened for cytotoxicity in a panel of colorectal, ovarian, and brain cancer cell lines. The selectivity of the compounds was assessed by determining the cytotoxicity in normal epithelial cell line (CHO). The most potent compound, 6j, was efficacious (with IC50 range of 0.6-1.2 μM) in colon (HCT116 and HCT15), brain (LN-229 and GBM-10) and ovarian (A2780 and OV2008) cancer cell lines. In contrast, in the normal cell line (CHO), the IC50 values for 6j were 14 ± 1...
July 20, 2017: European Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/28759042/inhibition-of-the-spindle-assembly-checkpoint-kinase-mps-1-as-a-novel-therapeutic-strategy-in-malignant-mesothelioma
#14
A Szymiczek, M Carbone, S Pastorino, A Napolitano, M Tanji, M Minaai, I Pagano, J M Mason, H I Pass, M R Bray, T W Mak, H Yang
Malignant mesothelioma (MM) is an aggressive malignancy, highly resistant to current medical and surgical therapies, whose tumor cells characteristically show a high level of aneuploidy and genomic instability. We tested our hypothesis that targeting chromosomal instability in MM would improve response to therapy. Thr/Tyr kinase (TTK)/monopolar spindle 1 kinase (Mps-1) is a kinase of the spindle assembly checkpoint that controls cell division and cell fate. CFI-402257 is a novel, selective inhibitor of Mps-1 with antineoplastic activity...
July 31, 2017: Oncogene
https://www.readbyqxmd.com/read/28749250/discovery-of-thalicthuberine-as-a-novel-antimitotic-agent-from-nature-that-disrupts-microtubule-dynamics-and-induces-apoptosis-in-prostate-cancer-cells
#15
Claire Levrier, Anja Rockstroh, Brian Gabrielli, Maria Kavallaris, Melanie Lehman, Rohan A Davis, Martin C Sadowski, Colleen C Nelson
We report for the first time the mechanism of action of the natural product thalicthuberine (TH) in prostate and cervical cancer cells. TH induced a strong accumulation of LNCaP cells in mitosis, severe mitotic spindle defects and asymmetric cell divisions, ultimately leading to mitotic catastrophe accompanied by cell death through apoptosis. However, unlike microtubule-binding drugs (vinblastine and paclitaxel), TH did not directly inhibit tubulin polymerization when tested in a cell-free system, whereas it reduced cellular microtubule polymer mass in LNCaP cells...
July 27, 2017: Cell Cycle
https://www.readbyqxmd.com/read/28725634/ip3-receptor-mediated-calcium-signaling-and-its-role-in-autophagy-in-cancer
#16
REVIEW
Elzbieta Kania, Gemma Roest, Tim Vervliet, Jan B Parys, Geert Bultynck
Calcium ions (Ca(2+)) play a complex role in orchestrating diverse cellular processes, including cell death and survival. To trigger signaling cascades, intracellular Ca(2+) is shuffled between the cytoplasm and the major Ca(2+) stores, the endoplasmic reticulum (ER), the mitochondria, and the lysosomes. A key role in the control of Ca(2+) signals is attributed to the inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs), the main Ca(2+)-release channels in the ER. IP3Rs can transfer Ca(2+) to the mitochondria, thereby not only stimulating core metabolic pathways but also increasing apoptosis sensitivity and inhibiting basal autophagy...
2017: Frontiers in Oncology
https://www.readbyqxmd.com/read/28720575/hsp72-and-nek6-cooperate-to-cluster-amplified-centrosomes-in-cancer-cells
#17
Josephina Sampson, Laura O'Regan, Martin J S Dyer, Richard Bayliss, Andrew M Fry
Cancer cells frequently possess extra amplified centrosomes clustered into two poles whose pseudo-bipolar spindles exhibit reduced fidelity of chromosome segregation and promote genetic instability. Inhibition of centrosome clustering triggers multipolar spindle formation and mitotic catastrophe, offering an attractive therapeutic approach to selectively kill cells with amplified centrosomes. However, mechanisms of centrosome clustering remain poorly understood. Here, we identify a new pathway that acts through NIMA-related kinase 6 (Nek6) and Hsp72 to promote centrosome clustering...
July 18, 2017: Cancer Research
https://www.readbyqxmd.com/read/28691904/synthetic-lethality-between-the-cohesin-subunits-stag1-and-stag2-in-diverse-cancer-contexts
#18
Petra van der Lelij, Simone Lieb, Julian Jude, Gordana Wutz, Catarina P Santos, Katrina Falkenberg, Andreas Schlattl, Jozef Ban, Raphaela Schwentner, Thomas Hoffmann, Heinrich Kovar, Francisco X Real, Todd Waldman, Mark A Pearson, Norbert Kraut, Jan-Michael Peters, Johannes Zuber, Mark Petronczki
Recent genome analyses have identified recurrent mutations in the cohesin complex in a wide range of human cancers. Here we demonstrate that the most frequently mutated subunit of the cohesin complex, STAG2, displays a strong synthetic lethal interaction with its paralog STAG1. Mechanistically, STAG1 loss abrogates sister chromatid cohesion in STAG2 mutated but not in wild-type cells leading to mitotic catastrophe, defective cell division and apoptosis. STAG1 inactivation inhibits the proliferation of STAG2 mutated but not wild-type bladder cancer and Ewing sarcoma cell lines...
July 10, 2017: ELife
https://www.readbyqxmd.com/read/28688972/suppression-of-angiogenesis-and-tumour-progression-by-combretastatin-and-derivatives
#19
G V Sherbet
The search for small molecule inhibitors has gained prominence with the recognition of their inherent advantage for cancer therapy. Combretastatin is a naturally occurring small stilbenoid. By virtue of the ability to bind to tubulin combretastatin and its derivatives promote depolymerisation of microtubules as well as inhibit tubulin polymerisation. This suppresses cell proliferation signalling and induces apoptosis. Combretastatins activate mitotic checkpoints that lead to mitotic catastrophe and apoptosis...
July 6, 2017: Cancer Letters
https://www.readbyqxmd.com/read/28686960/photodynamic-therapy-with-tmpyp-porphyrine-induces-mitotic-catastrophe-and-microtubule-disorganization-in-hela-and-g361-cells-a-comprehensive-view-of-the-action-of-the-photosensitizer
#20
Věra Cenklová
Photodynamic therapy (PDT) is a useful tool against cancer and various other diseases. PDT is capable to induce different cell death mechanisms, due to the PDT evoked reactive oxygen species (ROS) production and is dose dependent. It is known that cytoskeleton is responsible for numerous cell functions, including cell division, maintenance of cell shape, their adhesion ability and movement. PDT initiated redistribution and subsequent disintegration of cytoskeletal components that precedes cell death. Here was present our results in HeLa and G361 cells subjected to sublethal PDT treatments using α,β,χ,δ porphyrin-Tetrakis (1-methylpyridinium-4-yl) p-Toluenesulfonate porphyrin (TMPyP)...
June 27, 2017: Journal of Photochemistry and Photobiology. B, Biology
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