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https://www.readbyqxmd.com/read/28933366/the-role-of-the-mapk-signaling-topoisomerase-and-dietary-bioactives-in-controlling-cancer-incidence
#1
REVIEW
Khaled A Selim, Hend Abdelrasoul, Mohamed Aboelmagd, Ahmed M Tawila
Reactive oxygen species (ROS) are common products of mitochondrial oxidative phosphorylation, xenobiotics metabolism and are generated in response to several environmental stress conditions. Some of them play important biochemical roles in cellular signal transduction and gene transcription. On the other hand, ROS are known to be involved in a wide range of human diseases, including cancer. The excessive production of such ROS together with disruption of homeostasis detoxifying mechanisms can mediate a series of cellular oxidative stresses...
April 26, 2017: Diseases (Basel)
https://www.readbyqxmd.com/read/28927798/effect-of-charcoal-dextran-stripped-fetal-bovine-serum-on-in-vitro-development-of-bovine-embryos
#2
Ayman Mesalam, Rami Kong, Imran Khan, Mmr Chowdhury, Byung-Hyun Choi, Sung Woo Kim, Kyu-Woan Cho, Jong-In Jin, Il-Keun Kong
This study investigated the ability of charcoal:dextran stripped fetal bovine serum (CDS FBS) and heat-inactivated fetal bovine serum (HI FBS) to support in vitro development of bovine embryos. The developmental ability and quality of bovine embryos were determined by assessing their cell number, lipid content, mitochondrial activity, gene expression, and cryo-tolerance. The percentage of embryos that formed a blastocyst was significantly (P<0.05) higher in medium containing CDS FBS than in medium containing HI FBS (42...
September 16, 2017: Reproductive Biology
https://www.readbyqxmd.com/read/28927457/p53-key-conductor-of-all-anti-acne-therapies
#3
REVIEW
Bodo C Melnik
This review based on translational research predicts that the transcription factor p53 is the key effector of all anti-acne therapies. All-trans retinoic acid (ATRA) and isotretinoin (13-cis retinoic acid) enhance p53 expression. Tetracyclines and macrolides via inhibiting p450 enzymes attenuate ATRA degradation, thereby increase p53. Benzoyl peroxide and hydrogen peroxide elicit oxidative stress, which upregulates p53. Azelaic acid leads to mitochondrial damage associated with increased release of reactive oxygen species inducing p53...
September 19, 2017: Journal of Translational Medicine
https://www.readbyqxmd.com/read/28927142/tumour-growth-suppressive-effect-of-arsenic-trioxide-in-squamous-cell-lung-carcinoma
#4
Leanne Lee Leung, Sze-Kwan Lam, Yuan-Yuan Li, James Chung-Man Ho
Lung squamous cell carcinoma (SCC) is the second most common subtype of non-small cell lung carcinoma. The anticancer effects of arsenic trioxide (ATO) in lung adenocarcinoma and small-cell lung cancer have previously been reported; however its effects in SCC remain unclear. An MTT assay and western blot analysis were performed to determine cell viability and protein expression, respectively, in the SK-MES-1 and SW900 SCC cell lines following treatment with ATO. Phosphatidylserine externalization, mitochondrial membrane depolarization and cell cycle distribution were studied using flow cytometry and the in vivo effects of ATO on tumour growth were investigated with a xenograft model...
September 2017: Oncology Letters
https://www.readbyqxmd.com/read/28924186/interactome-analysis-reveals-znf804a-a-schizophrenia-risk-gene-as-a-novel-component-of-protein-translational-machinery-critical-for-embryonic-neurodevelopment
#5
Y Zhou, F Dong, T A Lanz, V Reinhart, M Li, L Liu, J Zou, H S Xi, Y Mao
Recent genome-wide association studies identified over 100 genetic loci that significantly associate with schizophrenia (SZ). A top candidate gene, ZNF804A, was robustly replicated in different populations. However, its neural functions are largely unknown. Here we show in mouse that ZFP804A, the homolog of ZNF804A, is required for normal progenitor proliferation and neuronal migration. Using a yeast two-hybrid genome-wide screen, we identified novel interacting proteins of ZNF804A. Rather than transcriptional factors, genes involved in mRNA translation are highly represented in our interactome result...
September 19, 2017: Molecular Psychiatry
https://www.readbyqxmd.com/read/28922540/ape1-ref-1-knockdown-in-pancreatic-ductal-adenocarcinoma-characterizing-gene-expression-changes-and-identifying-novel-pathways-using-single-cell-rna-sequencing
#6
Fenil Shah, Emery Goossens, Nadia M Atallah, Michelle Grimard, Mark R Kelley, Melissa L Fishel
Apurinic/apyrimidinic endonuclease 1/redox factor-1 (APE1/Ref-1 or APE1) is a multifunctional protein that regulates numerous transcription factors associated with cancer-related pathways. Because APE1 is essential for cell viability, generation of APE1 knockout cell lines and determining a comprehensive list of genes regulated by APE1 has not been possible. To circumvent this challenge, we utilized single-cell RNA Sequencing to identify differentially expressed genes in relation to APE1 protein levels within the cell...
September 18, 2017: Molecular Oncology
https://www.readbyqxmd.com/read/28920013/transcriptional-regulation-of-stem-cell-and-cancer-stem-cell-metabolism
#7
Ahmet Alptekin, Bingwei Ye, Han-Fei Ding
PURPOSE OF REVIEW: Metabolism is increasingly recognized as a major player in control of stem cell function and fate. How stem cell metabolism is established, maintained, and regulated is a fundamental question of biology and medicine. In this review, we discuss major metabolic programs in stem cells and cancer stem cells, with a focus on key transcription factors that shape the stem cell metabolic phenotype. RECENT FINDINGS: Cancer stem cells primarily use oxidative phosphorylation for energy generation, in contrast to normal stem cells, which rely on glycolytic metabolism with the exception of mouse embryonic stem cells...
March 2017: Current Stem Cell Reports
https://www.readbyqxmd.com/read/28918000/nitric-oxide-prevents-aft1-activation-and-metabolic-remodeling-in-frataxin-deficient-yeast
#8
David Alsina, Joaquim Ros, Jordi Tamarit
Yeast frataxin homolog (Yfh1) is the orthologue of human frataxin, a mitochondrial protein whose deficiency causes Friedreich Ataxia. Yfh1 deficiency activates Aft1, a transcription factor governing iron homeostasis in yeast cells. Although the mechanisms causing this activation are not completely understood, it is assumed that it may be caused by iron-sulfur deficiency. However, several evidences indicate that activation of Aft1 occurs in the absence of iron-sulfur deficiency. Besides, Yfh1 deficiency also leads to metabolic remodeling (mainly consisting in a shift from respiratory to fermentative metabolism) and to induction of Yhb1, a nitric oxide (NO) detoxifying enzyme...
September 6, 2017: Redox Biology
https://www.readbyqxmd.com/read/28915557/loss-of-p16-ink4a-stimulates-aberrant-mitochondrial-biogenesis-through-a-cdk4-rb-independent-pathway
#9
Ethika Tyagi, Bin Liu, Chelsea Li, Tong Liu, Jared Rutter, Douglas Grossman
The tumor suppressor p16INK4A (p16) inhibits cell cycle progression through the CDK4/Rb pathway. We have previously shown that p16 regulates cellular oxidative stress, independent of its role in cell cycle control. We investigated whether loss of p16 had a direct impact on the mitochondria. We found that p16-null primary mouse fibroblasts (PMFs) displayed increased mitochondrial mass and expression of mitochondrial respiratory subunit proteins compared to wild-type (WT) PMFs. These findings in p16-null PMFs were associated with increased expression of the mitochondrial biogenesis transcription factors PRC and TFAM...
August 22, 2017: Oncotarget
https://www.readbyqxmd.com/read/28912445/cofilin-mediated-neuronal-apoptosis-via-p53-translocation-and-pld1-regulation
#10
Tian Liu, Fang Wang, Patrick LePochat, Jung-A A Woo, Mohammed Zaheen Bukhari, Kyung Woo Hong, Courtney Trotter, David E Kang
Amyloid β (Aβ) accumulation is an early event in the pathogenesis of Alzheimer's disease (AD), leading to mitochondrial and synaptic dysfunction, tau accumulation, and eventual neuronal death. While the p53 apoptotic pathway has clearly been associated with Aβ deposits and neuronal apoptosis, the critical upstream factors contributing to p53 activation in AD are not well understood. We have previously shown that cofilin activation plays a pivotal role in Aβ-induced mitochondrial and synaptic dysfunction...
September 14, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28912168/alternative-polyadenylation-of-prelid1-regulates-mitochondrial-ros-signaling-and-cancer-outcomes
#11
Austin E Gillen, Heather M Brechbuhl, Tomomi M Yamamoto, Enos C Kline, Manoj Pillai, Jay Hesselberth, Peter Kabos
Disruption of post-transcriptional gene regulation is a critical step in oncogenesis that can be difficult to observe using traditional molecular techniques. To overcome this limitation, a modified polyadenylation site sequencing (PAS-seq) protocol was used to generate a genome-wide map of alternative polyadenylation (APA) events in human primary breast tumor specimens and matched normal tissue. This approach identified an APA event in the PRELID1 mRNA that enhances its steady state level and translational efficiency, and is a strong breast cancer subtype-dependent predictor of patient clinical outcomes...
September 14, 2017: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/28906435/mitochondrial-biogenesis-in-response-to-chromium-vi-toxicity-in-human-liver-cells
#12
Xiali Zhong, Rita de Cássia da Silveira E Sá, Caigao Zhong
Hexavalent chromium (Cr(VI)) is a ubiquitous environmental pollutant, which poses a threat to human public health. Recent studies have shown that mitochondrial biogenesis can be activated by inflammatory and oxidative stress. However, whether mitochondrial biogenesis is involved in Cr(VI)-induced hepatotoxicity is unclear. Here, we demonstrated the induction of inflammatory response and oxidative stress, as indicated by upregulation of inflammatory factors and reactive oxygen species (ROS). Subsequently, we demonstrated that mitochondrial biogenesis, comprising the mitochondrial DNA copy number and mitochondrial mass, was significantly increased in HepG2 cells exposed to low concentrations of Cr(VI)...
September 14, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28902841/cgas-senses-long-and-hmgb-tfam-bound-u-turn-dna-by-forming-protein-dna-ladders
#13
Liudmila Andreeva, Björn Hiller, Dirk Kostrewa, Charlotte Lässig, Carina C de Oliveira Mann, David Jan Drexler, Andreas Maiser, Moritz Gaidt, Heinrich Leonhardt, Veit Hornung, Karl-Peter Hopfner
Cytosolic DNA arising from intracellular pathogens triggers a powerful innate immune response. It is sensed by cyclic GMP-AMP synthase (cGAS), which elicits the production of type I interferons by generating the second messenger 2'3'-cyclic-GMP-AMP (cGAMP). Endogenous nuclear or mitochondrial DNA can also be sensed by cGAS under certain conditions, resulting in sterile inflammation. The cGAS dimer binds two DNA ligands shorter than 20 base pairs side-by-side, but 20-base-pair DNA fails to activate cGAS in vivo and is a poor activator in vitro...
September 13, 2017: Nature
https://www.readbyqxmd.com/read/28888871/interplay-of-mitochondria-apoptosis-regulatory-factors-and-micrornas-in-valvular-heart-disease
#14
Muhammad Ishtiaq Jan, Riaz Anwar Khan, Tahir Ali, Muhammad Bilal, Long Bo, Abdul Sajid, Abdul Malik, Naseeb Urehman, Nayyar Waseem, Javed Nawab, Murad Ali, Abdul Majeed, Hamid Ahmad, Sohail Aslam, Sadia Hamera, Aneesa Sultan, Mariam Anees, Qamar Javed, Iram Murtaza
Valvular heart disease (VHD) is an active process involving a wide range of pathological changes. The major complications of VHD are stenosis and regurgitation, which are macroscopic phenomena, induced in part through cellular changes. Altered expression of mitochondria associated genes causes membrane potential depolarization, leading to the increased levels of apoptosis observed in cardiac dysfunction. Objective of this study is to find molecular medicine candidates that can control expression of the key mitochondria apoptosis regulatory genes...
September 6, 2017: Archives of Biochemistry and Biophysics
https://www.readbyqxmd.com/read/28888048/involvement-of-nutrients-and-nutritional-mediators-in-mitochondrial-3-hydroxy-3-methylglutaryl-coa-synthase-gene-expression
#15
Tania Rescigno, Anna Capasso, Mario Felice Tecce
Mitochondrial 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase (HMGCS2) catalyses the first step of ketogenesis and is critical in various metabolic conditions. Several nutrient molecules were able to differentially modulate HMGCS2 expression levels. Docosahexaenoic acid (DHA, C22:6, n-3), eicosapentaenoic acid (EPA, C20:5, n-3), arachidonic acid (AA, C20:4, n-6) and glucose increased HMGCS2 mRNA and protein levels in HepG2 hepatoma cells, while fructose decreased them. The effect of n-6 AA resulted significantly higher than that of n-3 PUFA, but when combined all these molecules were far less efficient...
September 9, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28883902/sirt1-activation-by-resveratrol-alleviates-cardiac-dysfunction-via-mitochondrial-regulation-in-diabetic-cardiomyopathy-mice
#16
Sai Ma, Jing Feng, Ran Zhang, Jiangwei Chen, Dong Han, Xiang Li, Bo Yang, Xiujuan Li, Miaomiao Fan, Congye Li, Zuhong Tian, Yabin Wang, Feng Cao
BACKGROUND: Diabetic cardiomyopathy (DCM) is a major threat for diabetic patients. Silent information regulator 1 (SIRT1) has a regulatory effect on mitochondrial dynamics, which is associated with DCM pathological changes. Our study aims to investigate whether resveratrol, a SRIT1 activator, could exert a protective effect against DCM. METHODS AND RESULTS: Cardiac-specific SIRT1 knockout (SIRT1(KO)) mice were generated using Cre-loxP system. SIRT1(KO) mice displayed symptoms of DCM, including cardiac hypertrophy and dysfunction, insulin resistance, and abnormal glucose metabolism...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28877220/attenuated-lipotoxicity-and-apoptosis-is-linked-to-exogenous-and-endogenous-augmenter-of-liver-regeneration-by-different-pathways
#17
Thomas S Weiss, Madeleine Lupke, Sara Ibrahim, Christa Buechler, Julia Lorenz, Petra Ruemmele, Ute Hofmann, Michael Melter, Rania Dayoub
Nonalcoholic fatty liver disease (NAFLD) covers a spectrum from simple steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis. Free fatty acids (FFA) induce steatosis and lipo-toxicity and correlate with severity of NAFLD. In this study we aimed to investigate the role of exogenous and endogenous ALR (augmenter of liver regeneration) for FFA induced ER (endoplasmatic reticulum) -stress and lipoapoptosis. Primary human hepatocytes or hepatoma cells either treated with recombinant human ALR (rhALR, 15kDa) or expressing short form ALR (sfALR, 15kDa) were incubated with palmitic acid (PA) and analyzed for lipo-toxicity, -apoptosis, activation of ER-stress response pathways, triacylglycerides (TAG), mRNA and protein expression of lipid metabolizing genes...
2017: PloS One
https://www.readbyqxmd.com/read/28871145/reversible-keap1-inhibitors-are-preferential-pharmacological-tools-to-modulate-cellular-mitophagy
#18
Nikolaos D Georgakopoulos, Michele Frison, Maria Soledad Alvarez, Hélène Bertrand, Geoff Wells, Michelangelo Campanella
Mitophagy orchestrates the autophagic degradation of dysfunctional mitochondria preventing their pathological accumulation and contributing to cellular homeostasis. We previously identified a novel chemical tool (hereafter referred to as PMI), which drives mitochondria into autophagy without collapsing their membrane potential (ΔΨm). PMI is an inhibitor of the protein-protein interaction (PPI) between the transcription factor Nrf2 and its negative regulator, Keap1 and is able to up-regulate the expression of autophagy-associated proteins, including p62/SQSTM1...
September 4, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28864016/effects-of-maternal-diabetes-and-fetal-sex-on-human-placenta-mitochondrial-biogenesis
#19
Shaoning Jiang, April M Teague, Jeanie B Tryggestad, Christopher E Aston, Timothy Lyons, Steven D Chernausek
Abnormal placental function in maternal diabetes affects fetal health and can predispose offspring to metabolic diseases in later life. There are fetal sex-specific differences in placenta structure and gene expression, which may affect placental responses to maternal diabetes. The present study examined the effects of maternal diabetes on indices of mitochondrial biogenesis in placentae from male and female offspring. Mitochondrial DNA (mtDNA) copy number and expression of key regulators of mitochondrial biogenesis were assessed in placentae from 19 diabetic and 23 non-diabetic women...
September 2017: Placenta
https://www.readbyqxmd.com/read/28863367/monomeric-cocoa-catechins-enhance-%C3%AE-cell-function-by-increasing-mitochondrial-respiration
#20
Thomas J Rowley, Benjamin F Bitner, Jason D Ray, Daniel R Lathen, Andrew T Smithson, Blake W Dallon, Chase J Plowman, Benjamin T Bikman, Jason M Hansen, Melanie R Dorenkott, Katheryn M Goodrich, Liyun Ye, Sean F O'Keefe, Andrew P Neilson, Jeffery S Tessem
A hallmark of type 2 diabetes (T2D) is β-cell dysfunction and the eventual loss of functional β-cell mass. Therefore, mechanisms that improve or preserve β-cell function could be used to improve the quality of life of individuals with T2D. Studies have shown that monomeric, oligomeric and polymeric cocoa flavanols have different effects on obesity, insulin resistance and glucose tolerance. We hypothesized that these cocoa flavanols may have beneficial effects on β-cell function. INS-1 832/13-derived β-cells and primary rat islets cultured with a monomeric catechin-rich cocoa flavanol fraction demonstrated enhanced glucose-stimulated insulin secretion, while cells cultured with total cocoa extract and with oligomeric or polymeric procyanidin-rich fraction demonstrated no improvement...
July 27, 2017: Journal of Nutritional Biochemistry
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