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Mitotic catastrophe

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https://www.readbyqxmd.com/read/28725634/ip3-receptor-mediated-calcium-signaling-and-its-role-in-autophagy-in-cancer
#1
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
#2
Josephina Sampson, Laura O'Regan, Martin Js 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
#3
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
#4
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
#5
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
https://www.readbyqxmd.com/read/28670704/cyclin-k-dependent-regulation-of-aurora-b-affects-apoptosis-and-proliferation-by-induction-of-mitotic-catastrophe-in-prostate-cancer
#6
Sabrina Schecher, Britta Walter, Michael Falkenstein, Stephan Macher-Goeppinger, Philipp Stenzel, Kristina Krümpelmann, Boris Hadaschik, Sven Perner, Glen Kristiansen, Stefan Duensing, Wilfried Roth, Katrin E Tagscherer
Cyclin K plays a critical role in transcriptional regulation as well as cell development. However, the role of Cyclin K in prostate cancer is unknown. Here, we describe the impact of Cyclin K on prostate cancer cells and examine the clinical relevance of Cyclin K as a biomarker for patients with prostate cancer. We show that Cyclin K depletion in prostate cancer cells induces apoptosis and inhibits proliferation accompanied by an accumulation of cells in the G2/M phase. Moreover, knockdown of Cyclin K causes mitotic catastrophe displayed by multinucleation and spindle multipolarity...
July 3, 2017: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/28653883/the-nitric-oxide-donor-js-k-sensitizes-u87-glioma-cells-to-repetitive-irradiation
#7
Max Heckler, Nadja Osterberg, Jessica Guenzle, Nina Kristin Thiede-Stan, Wilfried Reichardt, Claudia Weidensteiner, Joseph E Saavedra, Astrid Weyerbrock
As a potent radiosensitizer nitric oxide (NO) may be a putative adjuvant in the treatment of malignant gliomas which are known for their radio- and chemoresistance. The NO donor prodrug JS-K (O2-(2.4-dinitrophenyl) 1-[(4-ethoxycarbonyl) piperazin-1-yl] diazen-1-ium-1,2-diolate) allows cell-type specific intracellular NO release via enzymatic activation by glutathione-S-transferases overexpressed in glioblastoma multiforme. The cytotoxic and radiosensitizing efficacy of JS-K was assessed in U87 glioma cells in vitro focusing on cell proliferation, induction of DNA damage, and cell death...
June 2017: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
https://www.readbyqxmd.com/read/28643424/mdm2-is-implicated-in-high-glucose-induced-podocyte-mitotic-catastrophe-via-notch1-signalling
#8
Hui Tang, Chun-Tao Lei, Chen Ye, Pan Gao, Cheng Wan, Shan Chen, Fang-Fang He, Yu-Mei Wang, Hua Su, Chun Zhang
Podocyte injury and depletion are essential events involved in the pathogenesis of diabetic nephropathy (DN). As a terminally differentiated cell, podocyte is restricted in 'post-mitosis' state and unable to regenerate. Re-entering mitotic phase will cause podocyte disastrous death which is defined as mitotic catastrophe (MC). Murine double minute 2 (MDM2), a cell cycle regulator, is widely expressed in renal resident cells including podocytes. Here, we explore whether MDM2 is involved in podocyte MC during hyperglycaemia...
June 23, 2017: Journal of Cellular and Molecular Medicine
https://www.readbyqxmd.com/read/28616577/caspase-2-in-mitotic-catastrophe-the-terminator-of-aneuploid-and-tetraploid-cells
#9
Ilio Vitale, Gwenola Manic, Maria Castedo, Guido Kroemer
Mitotic catastrophe is an oncosuppressive mechanism that targets cells experiencing defective mitoses via the activation of specific cell cycle checkpoints, regulated cell death pathways and/or cell senescence. This prevents the accumulation of karyotypic aberrations, which otherwise may drive oncogenesis and tumor progression. Here, we summarize experimental evidence confirming the role of caspase 2 (CASP2) as the main executor of mitotic catastrophe, and we discuss the signals that activate CASP2 in the presence of mitotic aberrations...
2017: Molecular & Cellular Oncology
https://www.readbyqxmd.com/read/28603525/modulating-both-tumor-cell-death-and-innate-immunity-is-essential-for-improving-radiation-therapy-effectiveness
#10
REVIEW
Qiuji Wu, Awatef Allouch, Isabelle Martins, Catherine Brenner, Nazanine Modjtahedi, Eric Deutsch, Jean-Luc Perfettini
Radiation therapy is one of the cornerstones of cancer treatment. In tumor cells, exposure to ionizing radiation (IR) provokes DNA damages that trigger various forms of cell death such as apoptosis, necrosis, autophagic cell death, and mitotic catastrophe. IR can also induce cellular senescence that could serve as an additional antitumor barrier in a context-dependent manner. Moreover, accumulating evidence has demonstrated that IR interacts profoundly with tumor-infiltrating immune cells, which cooperatively drive treatment outcomes...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28576750/bzml-a-novel-colchicine-binding-site-inhibitor-overcomes-multidrug-resistance-in-a549-taxol-cells-by-inhibiting-p-gp-function-and-inducing-mitotic-catastrophe
#11
Zhaoshi Bai, Meiqi Gao, Huijuan Zhang, Qi Guan, Jingwen Xu, Yao Li, Huan Qi, Zhengqiang Li, Daiying Zuo, Weige Zhang, Yingliang Wu
Multidrug resistance (MDR) interferes with the efficiency of chemotherapy. Therefore, developing novel anti-cancer agents that can overcome MDR is necessary. Here, we screened a series of colchicine binding site inhibitors (CBSIs) and found that 5-(3, 4, 5-trimethoxybenzoyl)-4-methyl-2-(p-tolyl) imidazol (BZML) displayed potent cytotoxic activity against both A549 and A549/Taxol cells. We further explored the underlying mechanisms and found that BZML caused mitosis phase arrest by inhibiting tubulin polymerization in A549 and A549/Taxol cells...
May 30, 2017: Cancer Letters
https://www.readbyqxmd.com/read/28572424/expression-of-concern-chromosomal-breaks-during-mitotic-catastrophe-trigger-%C3%AE-h2ax-atm-p53-mediated-apoptosis-gabriela-imreh-%C3%A2-helin-vakifahmetoglu-norberg-%C3%A2-stefan-imreh-%C3%A2-boris-zhivotovsky-j-cell-sci-%C3%A2-doi-%C3%A2-10-1242-jcs-081612
#12
https://www.readbyqxmd.com/read/28562324/prolonged-mitotic-arrest-induced-by-wee1-inhibition-sensitizes-breast-cancer-cells-to-paclitaxel
#13
Cody W Lewis, Zhigang Jin, Dawn Macdonald, Wenya Wei, Xu Jing Qian, Won Shik Choi, Ruicen He, Xuejun Sun, Gordon Chan
Wee1 kinase is a crucial negative regulator of Cdk1/cyclin B1 activity and is required for normal entry into and exit from mitosis. Wee1 activity can be chemically inhibited by the small molecule MK-1775, which is currently being tested in phase I/II clinical trials in combination with other anti-cancer drugs. MK-1775 promotes cancer cells to bypass the cell-cycle checkpoints and prematurely enter mitosis. In our study, we show premature mitotic cells that arise from MK-1775 treatment exhibited centromere fragmentation, a morphological feature of mitotic catastrophe that is characterized by centromeres and kinetochore proteins that co-cluster away from the condensed chromosomes...
May 13, 2017: Oncotarget
https://www.readbyqxmd.com/read/28550769/mk-8776-a-novel-chk1-inhibitor-exhibits-an-improved-radiosensitizing-effect-compared-to-ucn-01-by-exacerbating-radiation-induced-aberrant-mitosis
#14
Motofumi Suzuki, Tohru Yamamori, Tomoki Bo, Yuri Sakai, Osamu Inanami
Checkpoint kinase 1 (Chk1) is an evolutionarily conserved serine/threonine kinase that plays an important role in G2/M checkpoint signaling. Here, we evaluate the radiosensitizing effects of a novel selective Chk1 inhibitor MK-8776, comparing its efficacy with a first-generation Chk1 inhibitor UCN-01, and attempt to elucidate the mechanism of radiosensitization. In a clonogenic survival assay, MK-8776 demonstrated a more pronounced radiosensitizing effect than UCN-01, with lower cytotoxicity. Importantly, radiosensitization by MK-8776 can be achieved at doses as low as 2...
May 24, 2017: Translational Oncology
https://www.readbyqxmd.com/read/28536438/optimizing-radiotherapy-protocols-using-computer-automata-to-model-tumour-cell-death-as-a-function-of-oxygen-diffusion-processes
#15
Perrine Paul-Gilloteaux, Vincent Potiron, Grégory Delpon, Stéphane Supiot, Sophie Chiavassa, François Paris, Sylvain V Costes
The concept of hypofractionation is gaining momentum in radiation oncology centres, enabled by recent advances in radiotherapy apparatus. The gain of efficacy of this innovative treatment must be defined. We present a computer model based on translational murine data for in silico testing and optimization of various radiotherapy protocols with respect to tumour resistance and the microenvironment heterogeneity. This model combines automata approaches with image processing algorithms to simulate the cellular response of tumours exposed to ionizing radiation, modelling the alteration of oxygen permeabilization in blood vessels against repeated doses, and introducing mitotic catastrophe (as opposed to arbitrary delayed cell-death) as a means of modelling radiation-induced cell death...
May 23, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28534940/the-wnt-regulator-sfrp4-inhibits-mesothelioma-cell-proliferation-migration-and-antagonizes-wnt3a-via-its-netrin-like-domain
#16
Vanathi Perumal, Arun M Dharmarajan, Simon A Fox
Secreted frizzled related proteins (SFRPs) are a family of Wnt regulators which are frequently downregulated in cancers. In malignant mesothelioma (MM), downregulation of SFRP4 has been reported as a mechanism which contributes to aberrant activation of oncogenic Wnt signaling. Here we investigated the biological consequences of SFRP4 in two mesothelioma cell models where this protein is downregulated. We used recombinant SFRP4 and transient overexpression to study changes in proliferation, migration and downstream signaling...
May 18, 2017: International Journal of Oncology
https://www.readbyqxmd.com/read/28506135/emerging-cell-cycle-inhibitors-for-acute-myeloid-leukemia
#17
REVIEW
Abdallah Abou Zahr, Gautam Borthakur
AML therapy remains very challenging despite our increased understanding of its molecular heterogeneity. Outcomes with chemotherapy and targeted therapy remain poor. Targeting cell cycle regulators might complement chemotherapy and targeted therapy and help in improving outcomes. Areas covered: Here we cover the pre-clinical and clinical data for both for cyclin dependent kinase (CDK) and cell-cycle checkpoint inhibitors. While CDK inhibition can inhibit proliferation, checkpoint inhibitors can facilitate cell cycle progression in presence of DNA damage and can induce mitotic catastrophe...
June 2017: Expert Opinion on Emerging Drugs
https://www.readbyqxmd.com/read/28442587/combined-aurka-and-h3k9-methyltransferase-targeting-inhibits-cell-growth-by-inducing-mitotic-catastrophe
#18
Angela Mathison, Ann Salmonson, Mckenna Missfeldt, Jennifer Bintz, Monique Williams, Sarah Kossak, Asha Nair, Thiago M de Assuncao, Trace Christensen, Navtej Buttar, Juan Iovanna, Robert Huebert, Gwen Lomberk
The current integrative pathobiologic hypothesis states that pancreatic cancer (PDAC) develops and progresses in response to an interaction between known oncogenes and downstream epigenomic regulators. Congruently, this study tests a new combinatorial therapy based on the inhibition of the Aurora kinase A (AURKA) oncogene and one of its targets, the H3K9 methylation-based epigenetic pathway. This therapeutic combination is effective at inhibiting the in vitro growth of PDAC cells both, in monolayer culture systems, and in three-dimensional spheroids and organoids...
April 25, 2017: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/28415717/the-imidazoacridinone-c-1311-induces-p53-dependent-senescence-or-p53-independent-apoptosis-and-sensitizes-cancer-cells-to-radiation
#19
Anna Skwarska, Shaliny Ramachandran, Grzegorz Dobrynin, Katarzyna B Leszczynska, Ester M Hammond
C-1311 is a small molecule, which has shown promise in a number of pre-clinical and clinical studies. However, the biological response to C-1311 exposure is complicated and has been reported to involve a number of cell fates. Here, we investigated the molecular signaling which determines the response to C-1311 in both cancer and non-cancer cell lines. For the first time we demonstrate that the tumor suppressor, p53 plays a key role in cell fate determination after C-1311 treatment. In the presence of wild-type p53, cells exposed to C-1311 entered senescence...
May 9, 2017: Oncotarget
https://www.readbyqxmd.com/read/28415610/the-tubulin-inhibitor-mg-2477-induces-autophagy-regulated-cell-death-ros-accumulation-and-activation-of-foxo3-in-neuroblastoma
#20
Judith Hagenbuchner, Lorena Lungkofler, Ursula Kiechl-Kohlendorfer, Giampietro Viola, Maria Grazia Ferlin, Michael J Ausserlechner, Petra Obexer
Neuroblastoma is the most frequent extra-cranial solid tumor in children with still high mortality in stage M. Here we studied the tubulin-inhibitor MG-2477 as a possible therapeutic agent for neuroblastoma therapy and uncovered that MG-2477 induces death in neuroblastoma cells independent of PKB-activation status and stage. MG-2477 triggers within 30 minutes extensive autophagosome-formation that finally leads to cell death associated with mitotic catastrophe. Autophagy is critical for MG-2477-induced death and is regulated by the BH3-only protein PMAIP1/NOXA which sequesters the anti-apoptotic BCL2-protein BCLXL and thereby displaces and activates the autophagy-regulator BECN1/beclin1...
May 9, 2017: Oncotarget
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