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https://www.readbyqxmd.com/read/29115590/overexpression-of-lamin-b1-induces-mitotic-catastrophe-in-colon-cancer-lovo-cells-and-is-associated-with-worse-clinical-outcomes
#1
Magdalena Izdebska, Maciej Gagat, Alina Grzanka
Lamins are the major components of the nuclear lamina and play important roles in many cellular processes. The role of lamins in cancer development and progression is still unclear but it is known that reduced expression of lamin B1 has been observed in colon cancer. Thus, the aim of the present study was to elucidate the influence of LMNB1 upregulation on colon cancer cell line after treatment with 5-FU. The results indicate, that overexpression of LMNB1 induced dose-dependent cell death mainly by mitotic catastrophe pathway...
November 1, 2017: International Journal of Oncology
https://www.readbyqxmd.com/read/29109414/involvement-of-autophagy-in-the-outcome-of-mitotic-catastrophe
#2
Irina V Sorokina, Tatiana V Denisenko, Gabriela Imreh, Pyotr A Tyurin-Kuzmin, Vitaliy O Kaminskyy, Vladimir Gogvadze, Boris Zhivotovsky
Evading cell death is a major driving force for tumor progression that is one of the main problems in current cancer research. Mitotic catastrophe (MC) represents attractive platform compromising tumor resistance to current therapeutic modalities. MC appeared as onco-suppressive mechanism and is defined as a stage driving the cell to an irreversible destiny, i.e. cell death via apoptosis or necrosis. Our study highlights that MC induction in colorectal carcinoma cell lines ultimately leads to the autophagy followed by apoptosis...
November 6, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29107018/flubendazole-induces-mitotic-catastrophe-and-apoptosis-in-melanoma-cells
#3
K Čáňová, L Rozkydalová, D Vokurková, E Rudolf
Flubendazole (FLU) is a widely used anthelmintic drug belonging to benzimidazole group. Recently, several studies have been published demonstrating its potential to inhibit growth of various tumor cells including those derived from colorectal cancer, breast cancer or leukemia via several mechanisms. In the present study we have investigated cytotoxic effects of FLU on malignant melanoma using A-375, BOWES and RPMI-7951 cell lines representing diverse melanoma molecular types. In all three cell lines, FLU inhibited cell growth and proliferation and disrupted microtubule structure and function which was accompanied by dramatic changes in cellular morphology...
October 26, 2017: Toxicology in Vitro: An International Journal Published in Association with BIBRA
https://www.readbyqxmd.com/read/29092660/identification-of-dise-inducing-shrnas-by-monitoring-cellular-responses
#4
Monal Patel, Marcus E Peter
Off-target effects (OTE) are an undesired side effect of RNA interference (RNAi) caused by partial complementarity between the targeting siRNA and mRNAs other than the gene to be silenced. The death receptor CD95 and its ligand CD95L contain multiple sequences that when expressed as either si- or shRNAs kill cancer cells through a defined OTE that targets critical survival genes. Death induced by survival gene elimination (DISE) is characterized by specific morphological changes such as elongated cell shapes, senescence-like enlarged cells, appearance of large intracellular vesicles, release of mitochondrial ROS followed by activation of caspase-2, and induction of a necrotic form of mitotic catastrophe...
November 1, 2017: Cell Cycle
https://www.readbyqxmd.com/read/29040814/inhibiting-polo-like-kinase-1-plk1-enhances-radiosensitization-via-modulating-dna-repair-proteins-in-non-small-cell-lung-cancer
#5
Da Yao, Peigui Gu, Youyu Wang, Weibin Luo, Huiliang Chi, Jianjun Ge, Youhui Qian
To assure the faithful chromosome segregation, cells make use of the spindle assembly checkpoint (SAC), which can be activated in aneuploidy cancer cells. In this study, the efficacies of inhibiting Polo-like kinase 1 (PLK1) on the radiosensitization of non-small cell lung cancer (NSCLC) cells were studied. Clonogenic survival assay was performed to identify the effects of the PLK1 inhibitor on radiosensitivity within NSCLC cells. Mitotic catastrophe assessment was used to measure the cell death and γH2AX foci were utilized to assess the DNA double-strand breaks (DSB)...
October 17, 2017: Biochemistry and Cell Biology, Biochimie et Biologie Cellulaire
https://www.readbyqxmd.com/read/29016926/activation-of-wee1-confers-resistance-to-pi3k-inhibition-in-glioblastoma
#6
Shaofang Wu, Shuzhen Wang, Feng Gao, Luyuan Li, Siyuan Zheng, W K Alfred Yung, Dimpy Koul
Background: Oncogenic activation of phosphatidylinositol-3 kinase (PI3K) signaling plays a pivotal role in the development of glioblastoma (GBM). However, pharmacological inhibition of PI3K has so far not been therapeutically successful due to adaptive resistance through a rapid rewiring of cancer cell signaling. Here we identified that WEE1 is activated after transient exposure to PI3K inhibition and confers resistance to PI3K inhibition in GBM. Methods: Patient-derived glioma-initiating cells and established GBM cells were treated with PI3K inhibitor or WEE1 inhibitor alone or in combination, and cell proliferation was evaluated by CellTiter-Blue assay...
July 7, 2017: Neuro-oncology
https://www.readbyqxmd.com/read/28993779/natural-killer-cell-response-to-chemotherapy-stressed-cancer-cells-role-in-tumor-immunosurveillance
#7
REVIEW
Alessandra Zingoni, Cinzia Fionda, Cristiana Borrelli, Marco Cippitelli, Angela Santoni, Alessandra Soriani
Natural killer (NK) cells are innate cytotoxic lymphoid cells that actively prevent neoplastic development, growth, and metastatic dissemination in a process called cancer immunosurveillance. An equilibrium between immune control and tumor growth is maintained as long as cancer cells evade immunosurveillance. Therapies designed to kill cancer cells and to simultaneously sustain host antitumor immunity are an appealing strategy to control tumor growth. Several chemotherapeutic agents, depending on which drugs and doses are used, give rise to DNA damage and cancer cell death by means of apoptosis, immunogenic cell death, or other forms of non-apoptotic death (i...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28947974/selective-cytotoxicity-of-vanadium-complexes-on-human-pancreatic-ductal-adenocarcinoma-cell-line-by-inducing-necroptosis-apoptosis-and-mitotic-catastrophe-process
#8
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...
September 1, 2017: Oncotarget
https://www.readbyqxmd.com/read/28945288/thiopurine-induced-mitotic-catastrophe-in-rad51d-deficient-mammalian-cells
#9
Michael D Wyatt, Nicole M Reilly, Shikha Patel, Preeti Rajesh, Gary P Schools, Phillip G Smiraldo, Douglas L Pittman
Thiopurines are part of a clinical regimen used for the treatment of autoimmune disorders and childhood acute lymphoblastic leukemia. However, despite these successes, there are also unintended consequences such as therapy-induced cancer in long-term survivors. Therefore, a better understanding of cellular responses to thiopurines will lead to improved and personalized treatment strategies. RAD51D is an important component of homologous recombination (HR), and our previous work established that mammalian cells defective for RAD51D are more sensitive to the thiopurine 6-thioguanine (6TG) and have dramatically increased numbers of multinucleated cells and chromosome instability...
September 25, 2017: Environmental and Molecular Mutagenesis
https://www.readbyqxmd.com/read/28938460/huwe1-regulates-the-establishment-and-maintenance-of-spermatogonia-by-suppressing-dna-damage-response
#10
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 that includes the spermatogonial stem cells. However, the mechanisms underlying their establishment from gonocyte embryonic precursors and their maintenance thereafter remain largely unknown. In this study, 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 knockout gonocytes showed a decrease in mitotic re-entry, which inhibited their transition to spermatogonia...
November 1, 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
#11
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-j-cell-sci-doi-10-1242-jcs-081612
#12
Gabriela Imreh, Helin Vakifahmetoglu Norberg, Stefan Imreh, Boris Zhivotovsky
No abstract text is available yet for this article.
October 1, 2017: Journal of Cell Science
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
#13
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
#14
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
#15
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
#16
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
#17
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
#18
Cristina Ramos-Pérez, Jessel Ayra-Plasencia, Emiliano Matos-Perdomo, Michael Lisby, Grant W Brown, Félix Machín
Topoisomerase II (Top2) is an 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...
October 5, 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
#19
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 (TAOK) 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 to 15 nmol/L, 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
#20
Jennifer M Sahni, Sylvia S Gayle, Bryan M Webb, Kristen L Weber-Bonk, Darcie D Seachrist, Salendra Singh, Steven T Sizemore, Nicole A Restrepo, Gurkan Bebek, Peter C 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...
October 1, 2017: Cancer Research
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