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https://www.readbyqxmd.com/read/29895957/universal-response-in-the-rko-colon-cancer-cell-line-to-distinct-antimitotic-therapies
#1
Alexander Lorz, Dana-Adriana Botesteanu, Doron Levy
Both classic and newer antimitotics commonly induce a prolonged mitotic arrest in cell culture. During arrest, cells predominantly undergo one of two fates: cell death by apoptosis, or mitotic slippage and survival. To refine this binary description, a quantitative understanding of these cell responses is needed. Herein, we propose a quantitative description of the kinetics of colon carcinoma RKO cell fates in response to different antimitotics, using data from the single cell experiments of Gascoigne and Taylor (2008)...
June 12, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29895732/plagiochiline-a-inhibits-cytokinetic-abscission-and-induces-cell-death
#2
Nicole S Stivers, Ashraful Islam, Elsa M Reyes-Reyes, Lavona K Casson, José C Aponte, Abraham J Vaisberg, Gerald B Hammond, Paula J Bates
We previously reported on the isolation and biological activities of plagiochiline A ( 1 ), a 2,3-secoaromadendrane-type sesquiterpenoid from the Peruvian medicinal plant, Plagiochila disticha . This compound was found to have antiproliferative effects on a variety of solid tumor cell lines, as well as several leukemia cell lines. Other researchers have also noted the cytotoxicity of plagiochiline A (isolated from different plant species), but there are no prior reports regarding the mechanism for this bioactivity...
June 12, 2018: Molecules: a Journal of Synthetic Chemistry and Natural Product Chemistry
https://www.readbyqxmd.com/read/29882797/targeting-histone-deacetylases-with-natural-and-synthetic-agents-an-emerging-anticancer-strategy
#3
REVIEW
Amit Kumar Singh, Anupam Bishayee, Abhay K Pandey
Cancer initiation and progression are the result of genetic and/or epigenetic alterations. Acetylation-mediated histone/non-histone protein modification plays an important role in the epigenetic regulation of gene expression. Histone modification is controlled by the balance between histone acetyltransferase and (HAT) and histone deacetylase (HDAC) enzymes. Imbalance between the activities of these two enzymes is associated with various forms of cancer. Histone deacetylase inhibitors (HDACi) regulate the activity of HDACs and are being used in cancer treatment either alone or in combination with other chemotherapeutic drugs/radiotherapy...
June 6, 2018: Nutrients
https://www.readbyqxmd.com/read/29849448/1-methyl-4-phenylpyridinium-induced-death-of-differentiated-sh-sy5y-neurons-is-potentiated-by-cholesterol
#4
Anu Raju, Parasuram Jaisankar, Anupom Borah, Kochupurackal Parameswarannayar Mohanakumar
Background/Aims: Hypercholesterolemia is recently considered a risk factor for Parkinson's disease (PD), the most consistent neurodegenerative movement disorder. The study aimed to investigate the effect of exogenous cholesterol on 1-methyl-4-phenylpyridinium (MPP+ ) parkinsonian neurotoxin-induced cell death, loss of mitochondrial membrane potential, and dopaminergic deficiency in a cellular model of PD. Methods: Cholesterol (50 μM) when added in the culture media alone or in combination with MPP+ was studied in SH-SY5Y neuroblastoma cells...
May 2018: Annals of Neurosciences
https://www.readbyqxmd.com/read/29808012/switching-off-immp2l-signaling-drives-senescence-via-simultaneous-metabolic-alteration-and-blockage-of-cell-death
#5
Lifeng Yuan, Linhui Zhai, Lili Qian, De Huang, Yi Ding, Handan Xiang, Xiaojing Liu, J Will Thompson, Juan Liu, Yong-Han He, Xiao-Qiong Chen, Jing Hu, Qing-Peng Kong, Minjia Tan, Xiao-Fan Wang
Cellular senescence is a fundamental cell fate playing a significant role throughout the natural aging process. However, the molecular determinants distinguishing senescence from other cell-cycle arrest states such as quiescence and post-mitotic state, and the specified mechanisms underlying cell-fate decisions towards senescence versus cell death in response to cellular stress stimuli remain less understood. Employing multi-omics approaches, we revealed that switching off the specific mitochondrial processing machinery involving the peptidase IMMP2L serves as the foundation of the senescence program, which was also observed during the mammalian aging process...
May 28, 2018: Cell Research
https://www.readbyqxmd.com/read/29793167/improvement-of-neuronal-differentiation-by-carbon-monoxide-role-of-pentose-phosphate-pathway
#6
Ana S Almeida, Nuno L Soares, Catarina O Sequeira, Sofia A Pereira, Ursula Sonnewald, Helena L A Vieira
Over the last decades, the silent-killer carbon monoxide (CO) has been shown to also be an endogenous cytoprotective molecule able to inhibit cell death and modulate mitochondrial metabolism. Neuronal metabolism is mostly oxidative and neurons also use glucose for maintaining their anti-oxidant status by generation of reduced glutathione (GSH) via the pentose-phosphate pathway (PPP). It is established that neuronal differentiation depends on reactive oxygen species (ROS) generation and signalling, however there is a lack of information about modulation of the PPP during adult neurogenesis...
May 15, 2018: Redox Biology
https://www.readbyqxmd.com/read/29788155/phase-i-study-of-the-checkpoint-kinase-1-inhibitor-gdc-0575-in-combination-with-gemcitabine-in-patients-with-refractory-solid-tumors
#7
A Italiano, J R Infante, G I Shapiro, K N Moore, P M LoRusso, E Hamilton, S Cousin, M Toulmonde, S Postel-Vinay, S Tolaney, E M Blackwood, S Mahrus, F V Peale, X Lu, A Moein, J Epler, K DuPree, M Tagen, E R Murray, J L Schutzman, J O Lauchle, A Hollebecque, J-C Soria
Background: Checkpoint kinase 1 (Chk1) inhibition following chemotherapy-elicited DNA damage overrides cell cycle arrest and induces mitotic catastrophe and cell death. GDC-0575 is a highly-selective oral small-molecule Chk1 inhibitor that results in tumor shrinkage and growth delay in xenograft models. We evaluated the safety, tolerability, and pharmacokinetic properties of GDC-0575 alone and in combination with gemcitabine. Antitumor activity and Chk1 pathway modulation were assessed...
February 23, 2018: Annals of Oncology: Official Journal of the European Society for Medical Oncology
https://www.readbyqxmd.com/read/29784668/centrosome-linker-induced-tetraploid-segregation-errors-link-rhabdoid-phenotypes-and-lethal-colorectal-cancers
#8
Andrea Remo, Erminia Manfrin, Pietro Parcesepe, Alberto Ferrarini, Hye Seung Han, Mickys Ugnius, Carmelo Laudanna, Michele Simbolo, Donatella Malanga, Duarte Mendes Oliveira, Elisabetta Baritono, Tommaso Colangelo, Lina Sabatino, Jacopo Giuliani, Enrico Molinari, Marianna Garonzi, Luciano Xumerle, Massimo Delledonne, Guido Giordano, Claudio Ghimenton, Fortunato Lonardo, Fulvio D'angelo, Federica Grillo, Luca Mastracci, Giuseppe Viglietto, Michele Ceccarelli, Vittorio Colantuoni, Aldo Scarpa, Massimo Pancione
Centrosome anomalies contribute to tumorigenesis but it remains unclear how they are generated in lethal cancer phenotypes. Here, it is demonstrated that human microsatellite instable (MSI) and BRAF(V600E) mutant colorectal cancers with a lethal rhabdoid phenotype are characterized by inactivation of centrosomal functions. A splice site mutation that causes an unbalanced dosage of rootletin (CROCC), a centrosomal-linker component required for centrosome cohesion and separation at the chromosome 1p36.13 locus, resulted in abnormally shaped centrosomes in rhabdoid cells from human colon tissues...
May 21, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29752437/caspase-mediated-cleavage-of-the-centrosomal-proteins-during-apoptosis
#9
Mi Young Seo, Kunsoo Rhee
The centrosome is the major microtubule-organizing center and plays important roles in intracellular transport, cellular morphology, and motility. In mitotic cells, centrosomes function as spindle poles to pull a set of chromosomes into daughter cells. In quiescent cells, primary cilia are originated from the centrosomes. Given its involvement in various cellular processes, it is little surprising that the organelle would also participate in apoptotic events. However, it remains elusive how the centrosome changes in structure and organization during apoptosis...
May 11, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29735611/survivin-inhibitors-mitigate-chemotherapeutic-resistance-in-breast-cancer-cells-by-suppressing-genotoxic-nf-kappab-activation
#10
Wei Wang, Bo Zhang, Arul M Mani, Zhongzhi Wu, Yu Fan, Wei Li, Zhao-Hui Wu
Therapeutic resistance developed after chemotherapy and aggressive metastasis are the major causes for cancer-related death in triple negative breast cancer (TNBC) patients. Survivin is the smallest member of Inhibitor-of-Apoptosis Proteins (IAPs) family, which plays critical roles in cell division and cell survival. High expression levels of survivin have been associated with therapeutic resistance in various cancers. We recently developed a novel small molecule survivin inhibitor mimicking IAP-binding motif of second mitochondria-derived activator of caspase, which showed high potency in promoting survivin degradation...
May 7, 2018: Journal of Pharmacology and Experimental Therapeutics
https://www.readbyqxmd.com/read/29735529/global-loss-of-leucine-carboxyl-methyltransferase-1-causes-severe-defects-in-fetal-liver-hematopoiesis
#11
Jocelyn A Lee, Zhengqi Wang, Danielle Sambo, Kevin D Bunting, David C Pallas
Leucine Carboxyl Methyltransferase-1 (LCMT-1)3 methylates the carboxy-terminal leucine α-carboxyl group of the catalytic subunits of the protein phosphatase 2A (PP2A) subfamily of protein phosphatases, PP2Ac, PP4c, and PP6c. LCMT-1 differentially regulates the formation and function of a subset of the heterotrimeric complexes that PP2A and PP4 form with their regulatory subunits. Global LCMT-1 knockout causes embryonic lethality in mice, but LCMT-1 function in development is unknown. In the current study, we analyzed the effects of global LCMT-1 loss on embryonic development...
May 7, 2018: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29713275/the-novel-small-molecule-stk899704-promotes-senescence-of-the-human-a549-nsclc-cells-by-inducing-dna-damage-responses-and-cell-cycle-arrest
#12
Chan-Woo Park, Yesol Bak, Min-Je Kim, Ganipisetti Srinivasrao, Joonsung Hwang, Nak K Sung, Bo Yeon Kim, Jae-Hyuk Yu, Jin Tae Hong, Do-Young Yoon
The novel synthetic compound designated STK899704 (PubChem CID: 5455708) suppresses the proliferation of a broad range of cancer cell types. However, the details of its effect on lung cancer cells are unclear. We investigated the precise anticancer effect of STK899704 on senescence and growth arrest of A549 human non-small cell lung cancer (NSCLC) cells. STK899704 affected NSCLC cell cycle progression and decreased cell viability in a dose-dependent manner. Immunofluorescence staining revealed that STK899704 destabilized microtubules...
2018: Frontiers in Pharmacology
https://www.readbyqxmd.com/read/29710496/dehydrocostus-lactone-induces-prominent-apoptosis-in-kidney-distal-tubular-epithelial-cells-and-interstitial-fibroblasts-along-with-cell-cycle-arrest-in-ovarian-epithelial-cells
#13
Soma Shiva Nageswara Rao Singireesu, Sujan Kumar Mondal, Sunil Misra, Suresh Yerramsetty, Suresh Babu K
Dehydrocostus lactone (DHCL), a sesquiterpene lactone is well-known for its antiulcer, anti-hepatotoxic and anticancer activity. However, the studies concerning the safety/toxicity potential of DHCL toward the cells of normal origin remain unclear. The present study is aimed at investigating the toxicity potential of DHCL in renal distal tubular and interstitial fibroblast cell lines (MDCK and NRK-49F cells, respectively), and also in ovarian epithelial cell line (CHO cells). The MTT assay has predicted potential cytotoxic activity of DHCL against the cell line types with IC50 values of 0...
March 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/29689621/sall2-represses-cyclins-d1-and-e1-expression-and-restrains-g1-s-cell-cycle-transition-and-cancer-related-phenotypes
#14
Viviana E Hermosilla, Ginessa Salgado, Elizabeth Riffo, David Escobar, Matías I Hepp, Carlos Farkas, Mario Galindo, Violeta Morín, María A García-Robles, Ariel F Castro, Roxana Pincheira
SALL2 is a poorly characterized transcription factor that belongs to the Spalt-like family involved in development. Mutations on SALL2 have been associated with ocular coloboma and cancer. In cancers, SALL2 is deregulated and is proposed as a tumor suppressor in ovarian cancer. SALL2 has been implicated in stemness, cell death, proliferation, and quiescence. However, mechanisms underlying roles of SALL2 related to cancer remain largely unknown. Here, we investigated the role of SALL2 in cell proliferation using mouse embryo fibroblasts (MEFs) derived from Sall2-/- mice...
April 24, 2018: Molecular Oncology
https://www.readbyqxmd.com/read/29679654/the-vanillin-derivative-6-bromine-5-hydroxy-4-methoxybenzaldehyde-induces-aberrant-mitotic-progression-and-enhances-radio-sensitivity-accompanying-suppression-the-expression-of-plk1-in-esophageal-squamous-cell-carcinoma
#15
Meng-Meng Gu, Ming Li, Dexuan Gao, Lang-Huan Liu, Yue Lang, Si-Ming Yang, Hongling Ou, Bo Huang, Ping-Kun Zhou, Zeng-Fu Shang
Esophageal squamous cell carcinoma (ESCC) is the most common form of esophageal cancer in China. Since chemotherapy is the standard clinical intervention for advanced ESCC, the development of highly effective and minimal/non-toxic drugs is essential to improve the clinical outcome and prognosis of the patients. A novel derivative of vanillin, 6-bromine-5-hydroxy-4-methoxybenzaldehyde (BVAN08), has been recently reported to activate different cell death pathways in cancer cells. In this study, we demonstrate that BVAN08 exhibits a potent anti-proliferation effect on ESCC cells (TE-1 and ECA-109) by inhibiting the expression of PLK1, an important mitotic kinase...
June 1, 2018: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/29658881/negative-regulation-of-g2-m-by-atr-mei-41-chk1-grapes-facilitates-tracheoblast-growth-and-tracheal-hypertrophy-in-drosophila
#16
Amrutha Kizhedathu, Archit V Bagul, Arjun Guha
Imaginal progenitors in Drosophila are known to arrest in G2 during larval stages and proliferate thereafter. Here we investigate the mechanism and implications of G2 arrest in progenitors of the adult thoracic tracheal epithelium (tracheoblasts). We report that tracheoblasts pause in G2 for ~48-56 h and grow in size over this period. Surprisingly, tracheoblasts arrested in G2 express drivers of G2-M like Cdc25/String (Stg). We find that mechanisms that prevent G2-M are also in place in this interval. Tracheoblasts activate Checkpoint Kinase 1/Grapes (Chk1/Grp) in an ATR/mei-41-dependent manner...
April 16, 2018: ELife
https://www.readbyqxmd.com/read/29628886/u1-snrnp-alteration-and-neuronal-cell-cycle-reentry-in-alzheimer-disease
#17
REVIEW
Bing Bai
The aberrancy of U1 small nuclear ribonucleoprotein (snRNP) complex and RNA splicing has been demonstrated in Alzheimer's disease (AD). Importantly, the U1 proteopathy is AD-specific, widespread and early-occurring, thus providing a very unique clue to the AD pathogenesis. The prominent feature of U1 histopathology is its nuclear depletion and redistribution in the neuronal cytoplasm. According to the preliminary data, the initial U1 cytoplasmic distribution pattern is similar to the subcellular translocation of the spliceosome in cells undergoing mitosis...
2018: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/29618387/deregulation-of-the-spindle-assembly-checkpoint-is-associated-with-paclitaxel-resistance-in-ovarian-cancer
#18
Taryne Chong, Amila Sarac, Cindy Q Yao, Linda Liao, Nicola Lyttle, Paul C Boutros, John M S Bartlett, Melanie Spears
BACKGROUND: Ovarian cancer is the leading gynecologic cancer diagnosed in North America and because related symptoms are not disease specific, this often leads to late detection, an advanced disease state, and the need for chemotherapy. Ovarian cancer is frequently sensitive to chemotherapy at diagnosis but rapid development of drug resistance leads to disease progression and ultimately death in the majority of patients. RESULTS: We have generated paclitaxel resistant ovarian cell lines from their corresponding native cell lines to determine driver mechanisms of drug resistance using gene expression arrays...
April 4, 2018: Journal of Ovarian Research
https://www.readbyqxmd.com/read/29607498/1-l-mt-an-ido-inhibitor-prevented-colitis-associated-cancer-by-inducing-cdc20-inhibition-mediated-mitotic-death-of-colon-cancer-cells
#19
Xiuting Liu, Wei Zhou, Xin Zhang, Yang Ding, Qianming Du, Rong Hu
Indoleamine 2,3-dioxygenase 1 (IDO1), known as IDO, catabolizes tryptophan through kynurenine pathway, whose activity is correlated with impaired clinical outcome of colorectal cancer. Here we showed that 1-L-MT, a canonical IDO inhibitor, suppressed proliferation of human colorectal cancer cells through inducing mitotic death. Our results showed that inhibition of IDO decreased the transcription of CDC20, which resulted in G2/M cycle arrest of HCT-116 and HT-29. Furthermore, 1-L-MT induced mitochondria injuries and caused apoptotic cancer cells...
April 1, 2018: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/29605721/combined-inhibition-of-atr-and-wee1-as-a-novel-therapeutic-strategy-in-triple-negative-breast-cancer
#20
Juan Jin, Hehui Fang, Fang Yang, Wenfei Ji, Nan Guan, Zijia Sun, Yaqin Shi, Guohua Zhou, Xiaoxiang Guan
Triple negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer that poses a clinical challenge. Thus, new therapy strategies are urgently needed. The selective WEE1 inhibitor, AZD1775, has shown strong anti-proliferative effects on a variety of tumors. Here, we first demonstrate that inhibition of ATR by selective inhibitor AZD6738 can enhance AZD1775-caused growth inhibition in TNBC. Our results show that the enhanced cell death is attributed to repressed DNA damage repair and excessive replication stress, thereby causing increased DNA damage reflected by accumulation of the DNA double-strand-break marker γH2AX...
May 2018: Neoplasia: An International Journal for Oncology Research
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