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Senescence, cancer, autophagy

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https://www.readbyqxmd.com/read/28415717/the-imidazoacridinone-c-1311-induces-p53-dependent-senescence-or-p53-independent-apoptosis-and-sensitizes-cancer-cells-to-radiation
#1
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...
March 10, 2017: Oncotarget
https://www.readbyqxmd.com/read/28260023/silencing-bmi1-radiosensitizes-human-breast-cancer-cells-by-inducing-dna-damage-and-autophagy
#2
James Griffith, Daniel Andrade, Meghna Mehta, William Berry, Doris M Benbrook, Natarajan Aravindan, Terence S Herman, Rajagopal Ramesh, Anupama Munshi
Overexpression of BMI1 in human cancer cells, a member of the polycomb group of repressive complexes, correlates with advanced stage of disease, aggressive clinico-pathological behavior, poor prognosis, and resistance to radiation and chemotherapy. Studies have shown that experimental reduction of BMI1 protein level in tumor cells results in inhibition of cell proliferation, induction of apoptosis and/or senescence, and increased susceptibility to cytotoxic agents and radiation therapy. Although a role for BMI1 in cancer progression and its importance as a molecular target for cancer therapy has been established, information on the impact of silencing BMI1 in triple-negative breast cancer (TNBC) and its consequence on radiotherapy have not been well studied...
April 2017: Oncology Reports
https://www.readbyqxmd.com/read/28213398/foxo-integration-of-insulin-signaling-with-glucose-and-lipid-metabolism
#3
REVIEW
Sojin Lee, H Henry Dong
The forkhead box O family consists of FoxO1, FoxO3, FoxO4 and FoxO6 proteins in mammals. Expressed ubiquitously in the body, the four FoxO isoforms share in common the amino DNA-binding domain, known as 'forkhead box' domain. They mediate the inhibitory action of insulin or insulin-like growth factor on key functions involved in cell metabolism, growth, differentiation, oxidative stress, senescence, autophagy and aging. Genetic mutations in FoxO genes or abnormal expression of FoxO proteins are associated with metabolic disease, cancer or altered lifespan in humans and animals...
May 2017: Journal of Endocrinology
https://www.readbyqxmd.com/read/28209717/autophagy-metabolism-and-cancer
#4
Jessie Yanxiang Guo, Eileen White
Macroautophagy (autophagy hereafter) is a process that collects cytoplasmic components, particularly mitochondria, and degrades them in lysosomes. In mammalian systems, basal autophagy levels are normally low but are profoundly stimulated by starvation and essential for survival. Cancer cells up-regulate autophagy and can be more autophagy-dependent than most normal tissues. Genetic deficiency in essential autophagy genes in tumors in many autochthonous mouse models for cancer reduces tumor growth. In K-ras(G12D)-driven non-small cell lung cancer (NSCLC) and other models, autophagy sustains metabolism and survival...
February 16, 2017: Cold Spring Harbor Symposia on Quantitative Biology
https://www.readbyqxmd.com/read/28140789/p53-and-rad9-the-dna-damage-response-and-regulation-of-transcription-networks
#5
REVIEW
Howard B Lieberman, Sunil K Panigrahi, Kevin M Hopkins, Li Wang, Constantinos G Broustas
The way cells respond to DNA damage is important since inefficient repair or misrepair of lesions can have deleterious consequences, including mutation, genomic instability, neurodegenerative disorders, premature aging, cancer or death. Whether damage occurs spontaneously as a byproduct of normal metabolic processes, or after exposure to exogenous agents, cells muster a coordinated, complex DNA damage response (DDR) to mitigate potential harmful effects. A variety of activities are involved to promote cell survival, and include DNA repair, DNA damage tolerance, as well as transient cell cycle arrest to provide time for repair before entry into critical cell cycle phases, an event that could be lethal if traversal occurs while damage is present...
April 2017: Radiation Research
https://www.readbyqxmd.com/read/28068183/nucleolar-aggresomes-mediate-release-of-pericentric-heterochromatin-and-nuclear-destruction-of-genotoxically-treated-cancer-cells
#6
Kristine Salmina, Anda Huna, Inna Inashkina, Alexander Belyayev, Jekabs Krigerts, Ladislava Pastova, Alejandro Vazquez-Martin, Jekaterina Erenpreisa
The role of the nucleolus and autophagy in maintenance of nuclear integrity is poorly understood. In addition, the mechanisms of nuclear destruction in cancer cells senesced after conventional chemotherapy are unclear. In an attempt to elucidate these issues, we studied teratocarcinoma PA1 cells treated with Etoposide (ETO), focusing on the nucleolus. Following treatment, most cells enter G2 arrest, display persistent DNA damage and activate p53, senescence, and macroautophagy markers. 2-5 µm sized nucleolar aggresomes (NoA) containing fibrillarin (FIB) and damaged rDNA, colocalized with ubiquitin, pAMPK, and LC3-II emerge, accompanied by heterochromatin fragments, when translocated perinuclearly...
March 4, 2017: Nucleus
https://www.readbyqxmd.com/read/28030837/bafilomycin-a1-triggers-proliferative-potential-of-senescent-cancer-cells-in-vitro-and-in-nod-scid-mice
#7
Halina Was, Kamila Barszcz, Joanna Czarnecka, Agata Kowalczyk, Tytus Bernas, Ewelina Uzarowska, Paulina Koza, Agata Klejman, Katarzyna Piwocka, Bozena Kaminska, Eva Sikora
Anticancer therapies that induce DNA damage tend to trigger senescence in cancer cells, a process known as therapy-induced senescence (TIS). Such cells may undergo atypical divisions, thus contributing to tumor re-growth. Accumulation of senescent cancer cells reduces survival of patients after chemotherapy. As senescence interplays with autophagy, a dynamic recycling process, we sought to study whether inhibition of autophagy interferes with divisions of TIS cells. We exposed human colon cancer HCT116 cells to repeated cycles of a chemotherapeutic agent - doxorubicin (doxo) and demonstrated induction of hallmarks of TIS (e...
February 7, 2017: Oncotarget
https://www.readbyqxmd.com/read/27929731/autophagic-homeostasis-is-required-for-the-pluripotency-of-cancer-stem-cells
#8
Tanveer Sharif, Emma Martell, Cathleen Dai, Barry E Kennedy, Patrick Murphy, Derek R Clements, Youra Kim, Patrick W K Lee, Shashi A Gujar
Pluripotency is an important feature of cancer stem cells (CSCs) that contributes to self-renewal and chemoresistance. The maintenance of pluripotency of CSCs under various pathophysiological conditions requires a complex interaction between various cellular pathways including those involved in homeostasis and energy metabolism. However, the exact mechanisms that maintain the CSC pluripotency remain poorly understood. In this report, using both human and murine models of CSCs, we demonstrate that basal levels of autophagy are required to maintain the pluripotency of CSCs, and that this process is differentially regulated by the rate-limiting enzyme in the NAD(+) synthesis pathway NAMPT (nicotinamide phosphoribosyltransferase) and the transcription factor POU5F1/OCT4 (POU class 5 homeobox 1)...
February 2017: Autophagy
https://www.readbyqxmd.com/read/27920038/tgf-%C3%AE-family-signaling-in-the-control-of-cell-proliferation-and-survival
#9
Yun Zhang, Peter B Alexander, Xiao-Fan Wang
The transforming growth factor β (TGF-β) family controls many fundamental aspects of cellular behavior. With advances in the molecular details of the TGF-β signaling cascade and its cross talk with other signaling pathways, we now have a more coherent understanding of the cytostatic program induced by TGF-β. However, the molecular mechanisms are still largely elusive for other cellular processes that are regulated by TGF-β and determine a cell's proliferation and survival, apoptosis, dormancy, autophagy, and senescence...
December 5, 2016: Cold Spring Harbor Perspectives in Biology
https://www.readbyqxmd.com/read/27917193/dna-damage-response-and-autophagy-a-meaningful-partnership
#10
REVIEW
Aristides G Eliopoulos, Sophia Havaki, Vassilis G Gorgoulis
Autophagy and the DNA damage response (DDR) are biological processes essential for cellular and organismal homeostasis. Herein, we summarize and discuss emerging evidence linking DDR to autophagy. We highlight published data suggesting that autophagy is activated by DNA damage and is required for several functional outcomes of DDR signaling, including repair of DNA lesions, senescence, cell death, and cytokine secretion. Uncovering the mechanisms by which autophagy and DDR are intertwined provides novel insight into the pathobiology of conditions associated with accumulation of DNA damage, including cancer and aging, and novel concepts for the development of improved therapeutic strategies against these pathologies...
2016: Frontiers in Genetics
https://www.readbyqxmd.com/read/27890807/diosmin-induced-senescence-apoptosis-and-autophagy-in-breast-cancer-cells-of-different-p53-status-and-erk-activity
#11
Anna Lewinska, Jagoda Adamczyk-Grochala, Ewa Kwasniewicz, Anna Deregowska, Maciej Wnuk
Relatively low bioavailability of plant-derived nutraceuticals with anticancer properties may limit their usefulness for prevention and therapy of cancer. In the present study, we have screened for nutraceuticals (n=30) that would act at low micromolar range against phenotypically distinct breast cancer cell lines, namely MCF-7 (ER(+), PR(+/-), HER2(-)), MDA-MB-231 (ER(-), PR(-), HER2(-)) and SK-BR-3 (ER(-), PR(-), HER2(+)), and diosmin, a citrus fruit flavonoid belonging to a flavone subclass, was selected...
January 4, 2017: Toxicology Letters
https://www.readbyqxmd.com/read/27812870/autophagy-detection-during-oncogene-induced-senescence-using-fluorescence-microscopy
#12
Masako Narita, Masashi Narita
Oncogene-induced senescence (OIS) is a highly dynamic process, involving several different effector mechanisms, the multitude and combination of which likely determines the quality of the phenotype (Pérez-Mancera et al., Nat Rev Cancer 14:547-558, 2014). Autophagy, a cellular degradation process, has been proposed to be one of these senescence effectors, although its functional relevance seems highly context dependent (Hoare et al., Semin Cancer Biol 21:397-404, 2011). A number of methods for monitoring autophagy are available, and several excellent protocols have been published in this journal (Klionsky et al...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/27775833/targeting-deubiquitinating-enzymes-in-glioblastoma-multiforme-expectations-and-challenges
#13
REVIEW
Wei-Lin Jin, Xiao-Yuan Mao, Guan-Zhong Qiu
Glioblastoma (GBM) is regarded as the most common primary intracranial neoplasm. Despite standard treatment with tumor resection and radiochemotherapy, the outcome remains gloomy. It is evident that a combination of oncogenic gain of function and tumor-suppressive loss of function has been attributed to glioma initiation and progression. The ubiquitin-proteasome system is a well-orchestrated system that controls the fate of most proteins by striking a dynamic balance between ubiquitination and deubiquitination of substrates, having a profound influence on the modulation of oncoproteins, tumor suppressors, and cellular signaling pathways...
October 24, 2016: Medicinal Research Reviews
https://www.readbyqxmd.com/read/27713168/the-aurora-kinase-a-inhibitor-tc-a2317-disrupts-mitotic-progression-and-inhibits-cancer-cell-proliferation
#14
Yoo Hong Min, Wootae Kim, Ja-Eun Kim
Mitotic progression is crucial for the maintenance of chromosomal stability. A proper progression is ensured by the activities of multiple kinases. One of these enzymes, the serine/threonine kinase Aurora A, is required for proper mitosis through the regulation of centrosome and spindle assembly. In this study, we functionally characterized a newly developed Aurora kinase A inhibitor, TC-A2317. In human lung cancer cells, TC-A2317 slowed proliferation by causing aberrant formation of centrosome and microtubule spindles and prolonging the duration of mitosis...
October 4, 2016: Oncotarget
https://www.readbyqxmd.com/read/27671304/dehydroleucodine-induces-a-tp73-dependent-transcriptional-regulation-of-multiple-cell-death-target-genes-in-human-glioblastoma-cells
#15
Edward A Ratovitski
Dehydroleucodine (DhL), a natural sesquiterpene lactone from Artemisia douglassiana Besser (Argentine) and Gynoxys verrucosa (Ecuador) was shown to induce a cell death in cancer cells through senescence, apoptosis, and DNA damage. Here, we found that the DhL exposure upregulated the total and phosphorylated (p-Y99) levels of TP73 in human glioblastoma U87-MG cells. We further found that TP73 silencing led to a partial rescue of U87-MG cells from the cell death induced by DhL. Upon the DhL exposure numerous gene targets were upregulated and downregulated through a TP73-dependent transcriptional mechanism...
September 23, 2016: Anti-cancer Agents in Medicinal Chemistry
https://www.readbyqxmd.com/read/27669643/the-regrowth-kinetic-of-the-surviving-population-is-independent-of-acute-and-chronic-responses-to-temozolomide-in-glioblastoma-cell-lines
#16
Andrew Oliveira Silva, Eloisa Dalsin, Giovana Ravizzoni Onzi, Eduardo Cremonese Filippi-Chiela, Guido Lenz
Chemotherapy acts on cancer cells by producing multiple effects on a cell population including cell cycle arrest, necrosis, apoptosis and senescence. However, often a subpopulation of cells survives and the behavior of this subpopulation, which is responsible for cancer recurrence, remains obscure. Here we investigated the in vitro short- and long-term responses of six glioblastoma cell lines to clinically relevant doses of temozolomide for 5 days followed by 23 days of recovery, mimicking the standard schedule used in glioblastoma patient for this drug...
September 23, 2016: Experimental Cell Research
https://www.readbyqxmd.com/read/27666934/mirnas-in-melanoma-tumor-suppressors-and-oncogenes-with-prognostic-potential
#17
REVIEW
Michal Wozniak, Aleksandra Mielczarek, Malgorzata Czyz
MicroRNAs (miRNAs), which are small non-coding RNA molecules that post-transcriptionally regulate the expression of target genes, control the vast majority of cellular events, including proliferation, differentiation, survival, senescence, autophagy, metabolism and genome stability. Even slight alterations in miRNA expression levels may induce the development of pathological states, including cancer. Several studies have already demonstrated the importance of miRNAs in the regulation of melanocytes. Upregulation of oncogenic miRNAs (oncomiRs), mainly by amplification and translocation of miRNA genes, and downregulation of oncosuppressor miRNAs (anti-oncomiRs) by deletion and other mutations, promoter methylation and abnormal processing contributes to melanoma initiation and progression...
2016: Current Medicinal Chemistry
https://www.readbyqxmd.com/read/27665945/rapamycin-and-fructose-1-6-bisphosphate-reduce-the-hepg2-cell-proliferation-via-increase-of-free-radicals-and-apoptosis
#18
Elisa Feller Gonçalves da Silva, Gabriele Catyana Krause, Kelly Goulart Lima, Gabriela Viegas Haute, Leonardo Pedrazza, Fernanda Cristina Mesquita, Bruno Souza Basso, Anderson Catarina Velasquez, Fernanda Bordignon Nunes, Jarbas Rodrigues de Oliveira
Hepatocellular carcinoma is the most prevalent type of tumor among primary tumors affecting the liver. Rapamycin is currently used as a basis for chemotherapy in the treatment of cancers, including the liver. Because it shows several adverse effects, minimizing these effects without compromising efficacy is important. In this sense other drugs may be used concomitantly. One of these drugs is fructose-1,6-bisphosphate (FBP), which has shown therapeutic effect in various pathological situations, having antioxidant and anti-inflammatory proprieties...
November 2016: Oncology Reports
https://www.readbyqxmd.com/read/27664235/recent-insights-into-the-function-of-autophagy-in-cancer
#19
Ravi Amaravadi, Alec C Kimmelman, Eileen White
Macroautophagy (referred to here as autophagy) is induced by starvation to capture and degrade intracellular proteins and organelles in lysosomes, which recycles intracellular components to sustain metabolism and survival. Autophagy also plays a major homeostatic role in controlling protein and organelle quality and quantity. Dysfunctional autophagy contributes to many diseases. In cancer, autophagy can be neutral, tumor-suppressive, or tumor-promoting in different contexts. Large-scale genomic analysis of human cancers indicates that the loss or mutation of core autophagy genes is uncommon, whereas oncogenic events that activate autophagy and lysosomal biogenesis have been identified...
September 1, 2016: Genes & Development
https://www.readbyqxmd.com/read/27618777/utility-of-the-dual-specificity-protein-kinase-ttk-as-a-therapeutic-target-for-intrahepatic-spread-of-liver-cancer
#20
Ruoyu Miao, Yan Wu, Haohai Zhang, Huandi Zhou, Xiaofeng Sun, Eva Csizmadia, Lian He, Yi Zhao, Chengyu Jiang, Rebecca A Miksad, Tahereh Ghaziani, Simon C Robson, Haitao Zhao
Therapies for primary liver cancer, the third leading cause of cancer-related death worldwide, remain limited. Following multi-omics analysis (including whole genome and transcriptome sequencing), we were able to identify the dual-specific protein kinase TTK as a putative new prognostic biomarker for liver cancer. Herein, we show that levels of TTK protein are significantly elevated in neoplastic tissues from a cohort of liver cancer patients, when compared with adjacent hepatic tissues. We also tested the utility of TTK targeted inhibition and have demonstrated therapeutic potential in an experimental model of liver cancer in vivo...
September 13, 2016: Scientific Reports
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