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EMT metabolism

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https://www.readbyqxmd.com/read/29677166/in-vitro-identification-of-new-transcriptomic-and-mirnomic-profiles-associated-with-pulmonary-fibrosis-induced-by-high-doses-everolimus-looking-for-new-pathogenetic-markers-and-therapeutic-targets
#1
Simona Granata, Gloria Santoro, Valentina Masola, Paola Tomei, Fabio Sallustio, Paola Pontrelli, Matteo Accetturo, Nadia Antonucci, Pierluigi Carratù, Antonio Lupo, Gianluigi Zaza
The administration of Everolimus (EVE), a mTOR inhibitor used in transplantation and cancer, is often associated with adverse effects including pulmonary fibrosis. Although the underlying mechanism is not fully clarified, this condition could be in part caused by epithelial to mesenchymal transition (EMT) of airway cells. To improve our knowledge, primary bronchial epithelial cells (BE63/3) were treated with EVE (5 and 100 nM) for 24 h. EMT markers (α-SMA, vimentin, fibronectin) were measured by RT-PCR. Transepithelial resistance was measured by Millicell-ERS ohmmeter...
April 20, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29665787/valproic-acid-sensitizes-metformin-resistant-human-renal-cell-carcinoma-cells-by-upregulating-h3-acetylation-and-emt-reversal
#2
Muyun Wei, Shaowei Mao, Guoliang Lu, Liang Li, Xiaopeng Lan, Zhongxian Huang, Yougen Chen, Miaoqing Zhao, Yueran Zhao, Qinghua Xia
BACKGROUND: Metformin (Met) is a widely available diabetic drug and shows suppressed effects on renal cell carcinoma (RCC) metabolism and proliferation. Laboratory studies in RCC suggested that metformin has remarkable antitumor activities and seems to be a potential antitumor drug. But the facts that metformin may be not effective in reducing the risk of RCC in cancer clinical trials made it difficult to determine the benefits of metformin in RCC prevention and treatment. The mechanisms underlying the different conclusions between laboratory experiments and clinical analysis remains unclear...
April 17, 2018: BMC Cancer
https://www.readbyqxmd.com/read/29644357/the-inhibitory-effect-of-manuka-honey-on-human-colon-cancer-hct-116-and-lovo-cell-growth-part-2-induction-of-oxidative-stress-alteration-of-mitochondrial-respiration-and-glycolysis-and-suppression-of-metastatic-ability
#3
Sadia Afrin, Francesca Giampieri, Massimiliano Gasparrini, Tamara Y Forbes-Hernández, Danila Cianciosi, Patricia Reboredo-Rodriguez, Piera Pia Manna, Jiaojiao Zhang, Josè L Quiles, Maurizio Battino
Despite its high content of phenolic compounds, the chemopreventive activity of Manuka honey (MH) is still elusive. The aim of the present work was to evaluate the effects of MH on oxidative stress, antioxidant enzymes, cellular metabolism and the metastatic ability in HCT-116 and LoVo cells, paying particular attention to the molecular mechanisms involved. We observed a strong induction of oxidative stress after MH treatment since it augmented the accumulation of reactive oxygen species and increased the damage to proteins, lipids and DNA...
April 12, 2018: Food & Function
https://www.readbyqxmd.com/read/29629336/deciphering-the-dichotomous-effects-of-pgc-1%C3%AE-on-tumorigenesis-and-metastasis
#4
REVIEW
Simon-Pierre Gravel
Metabolic reprogramming confers cancer cells the ability to grow and survive under nutrient-depleted or stressful microenvironments. The amplification of oncogenes, the loss of tumor suppressors, as well as context- and lineage-specific determinants can converge and profoundly affect the metabolic status of cancer cells. Cumulating evidences suggest that highly glycolytic cells under the influence of oncogenes such as BRAF, or evolving in hypoxic microenvironments, will promote metastasis through modulation of multiple steps of tumorigenesis such as the epithelial-to-mesenchymal transition (EMT)...
2018: Frontiers in Oncology
https://www.readbyqxmd.com/read/29581852/rhoa-rho-kinase-triggers-epithelial-mesenchymal-transition-in-mesothelial-cells-and-contributes-to-the-pathogenesis-of-dialysis-related-peritoneal-fibrosis
#5
Qinglian Wang, Xiaowei Yang, Ying Xu, Zhenwei Shen, Hongxia Cheng, Fajuan Cheng, Xiang Liu, Rong Wang
Peritoneal fibrosis (PF) with associated peritoneal dysfunction is almost invariably observed in long-term peritoneal dialysis (PD) patients. Advanced glycation end products (AGEs) are pro-oxidant compounds produced in excess during the metabolism of glucose and are present in high levels in standard PD solutions. The GTPase RhoA has been implicated in PF, but its specific role remains poorly understood. Here, we studied the effects of RhoA/Rho-kinase signaling in AGEs-induced epithelial-mesenchymal transition (EMT) in human peritoneal mesothelial cells (HPMCs), and evaluated morphological and molecular changes in a rat model of PD-related PF...
March 6, 2018: Oncotarget
https://www.readbyqxmd.com/read/29562686/profiling-prostate-cancer-therapeutic-resistance
#6
REVIEW
Cameron A Wade, Natasha Kyprianou
The major challenge in the treatment of patients with advanced lethal prostate cancer is therapeutic resistance to androgen-deprivation therapy (ADT) and chemotherapy. Overriding this resistance requires understanding of the driving mechanisms of the tumor microenvironment, not just the androgen receptor (AR)-signaling cascade, that facilitate therapeutic resistance in order to identify new drug targets. The tumor microenvironment enables key signaling pathways promoting cancer cell survival and invasion via resistance to anoikis...
March 19, 2018: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/29536528/clca2-epigenetic-regulation-by-ctbp1-hdacs-zeb1-ep300-and-mir-196b-5p-impacts-prostate-cancer-cell-adhesion-and-emt-in-metabolic-syndrome-disease
#7
Juliana Porretti, Guillermo N Dalton, Cintia Massillo, Georgina D Scalise, Paula L Farré, Randolph Elble, Esther N Gerez, Paula Accialini, Ana M Cabanillas, Kevin Gardner, Paola De Luca, Adriana De Siervi
Prostate cancer (PCa) is the most common cancer among men. Metabolic syndrome (MeS) is associated with increased PCa aggressiveness and recurrence. Previously, we proposed C-terminal binding protein 1 (CTBP1), a transcripcional co-repressor, as a molecular link between these two conditions. Notably, CTBP1 depletion decreased PCa growth in MeS mice. The aim of this study was to investigate the molecular mechanisms that explain the link between MeS and PCa mediated by CTBP1. We found that CTBP1 repressed Chloride Channel Accessory 2 (CLCA2) expression in prostate xenografts developed in MeS animals...
March 14, 2018: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/29504907/hk3-overexpression-associated-with-epithelial-mesenchymal-transition-in-colorectal-cancer
#8
Elena A Pudova, Anna V Kudryavtseva, Maria S Fedorova, Andrew R Zaretsky, Dmitry S Shcherbo, Elena N Lukyanova, Anatoly Y Popov, Asiya F Sadritdinova, Ivan S Abramov, Sergey L Kharitonov, George S Krasnov, Kseniya M Klimina, Nadezhda V Koroban, Nadezhda N Volchenko, Kirill M Nyushko, Nataliya V Melnikova, Maria A Chernichenko, Dmitry V Sidorov, Boris Y Alekseev, Marina V Kiseleva, Andrey D Kaprin, Alexey A Dmitriev, Anastasiya V Snezhkina
BACKGROUND: Colorectal cancer (CRC) is a common cancer worldwide. The main cause of death in CRC includes tumor progression and metastasis. At molecular level, these processes may be triggered by epithelial-mesenchymal transition (EMT) and necessitates specific alterations in cell metabolism. Although several EMT-related metabolic changes have been described in CRC, the mechanism is still poorly understood. RESULTS: Using CrossHub software, we analyzed RNA-Seq expression profile data of CRC derived from The Cancer Genome Atlas (TCGA) project...
February 9, 2018: BMC Genomics
https://www.readbyqxmd.com/read/29453983/aldolase-a-overexpression-is-associated-with-poor-prognosis-and-promotes-tumor-progression-by-the-epithelial-mesenchymal-transition-in-colon-cancer
#9
Feng Ye, Yixing Chen, Lu Xia, Jiabian Lian, Shuyu Yang
There is increasing evidence that glycolysis is involved in cancer progression. Aldolase is a glycolytic enzyme that catalyzes the reversible conversion of fructose-1,6-bisphosphate to glyceraldehyde-3-phosphate and dihydroxyacetone phosphate. Disruption of the aldolase genes also plays a role in the progression of multiple types of cancer. However, the underlying mechanism of the action of aldolases in colon cancer progression remains elusive. In this study, aldolase A expression was investigated and found to be upregulated along with human colon cancer progression and metastasis at both the mRNA and protein levels in human colon cancer tissues...
February 14, 2018: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/29453319/leptin-signaling-mediates-obesity-associated-csc-enrichment-and-emt-in-preclinical-tnbc-models
#10
Laura W Bowers, Emily L Rossi, Shannon B McDonell, Steven S Doerstling, Subreen A Khatib, Claire G Lineberger, Jody E Albright, Xiaohu Tang, Linda A deGraffenried, Stephen D Hursting
Obesity is associated with poor prognosis in triple-negative breast cancer (TNBC). Preclinical models of TNBC were used to test the hypothesis that increased leptin signaling drives obesity-associated TNBC development by promoting cancer stem cell (CSC) enrichment and/or epithelial-to-mesenchymal transition (EMT). MMTV-Wnt-1 transgenic mice, which develop spontaneous basal-like, triple-negative mammary tumors, received either a control diet (10% kcal from fat) or a diet-induced obesity regimen (DIO, 60% kcal from fat) for up to 42 weeks (n=15/group)...
February 16, 2018: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/29446048/adiponectin-and-colon-cancer-evidence-for-inhibitory-effects-on-viability-and-migration-of-human-colorectal-cell-lines
#11
E Nigro, P Schettino, R Polito, O Scudiero, M L Monaco, G D De Palma, A Daniele
Adiponectin (Acrp30) is an adipokine widely studied for its beneficial metabolic and anti-inflammatory properties. Colorectal cancer is among the most common cancers worldwide. The aim of present study was to explore the effects of Acrp30 on both CaCo-2 and HCT116 colorectal cancer cells in terms of viability, oxidative stress, and apoptosis. In addition, since colorectal cancer represents a typical inflammation-related cancer, we investigated whether Acrp30 treatment modifies the migration and the expression of crucial proteins in the EMT transition...
February 14, 2018: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/29439261/metabolomics-reveals-protection-of-resveratrol-in-diet-induced-metabolic-risk-factors-in-abdominal-muscle
#12
Guoyou Chen, Guozhu Ye, Xinbo Zhang, Xiaoxiao Liu, Yingfeng Tu, Zengjie Ye, Jincheng Liu, Qi Guo, Zhiguo Wang, Lin Wang, Sijun Dong, Yuhua Fan
BACKGROUND/AIMS: Abdominal obesity is recognized as the main reason of metabolic syndrome, which is closely related to disordered skeletal and/or abdominal muscle metabolic functions. Metabolomics is a comprehensive assessment system in biological metabolites. The aim of our present study is to investigate the diet-induced metabolic risk factors by metabolic in the abdominal muscles and clarify the relationship between atheroprotective effects of Resveratrol (Rev) and abdominal muscles metabolic components during the development of atherosclerosis...
2018: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/29416718/ing5-differentially-regulates-protein-lysine-acetylation-and-promotes-p300-autoacetylation
#13
Tao Zhang, Jin Meng, Xinli Liu, Xutao Zhang, Xiaojun Peng, Zhongyi Cheng, Feng Zhang
ING5 belongs to the Inhibitor of Growth (ING) candidate tumor suppressor family. Previously, we have shown that ING5 inhibits invasiveness of lung cancer cells by downregulating EMT-inducing genes. However, the underlying mechanisms remain unclear. The aim of the study was to use integrated approach involving SILAC labeling and mass spectrometry-based quantitative proteomics to quantify dynamic changes of acetylation regulated by ING5 in lung cancer cells. Here, we have found that ING5 has a profound influence on protein lysine acetylation with 163 acetylation peptides on 122 proteins significantly upregulated and 100 acetylation peptides on 72 proteins downregulated by ING5 overexpression...
January 5, 2018: Oncotarget
https://www.readbyqxmd.com/read/29393429/notch-signaling-molecule-is-involved-in-the-invasion-of-miapaca2-cells-induced-by-cocl2-via-regulating-epithelial%C3%A2-mesenchymal-transition
#14
Ding-Wei Chen, Hong Wang, Ya-Fang Bao, Kun Xie
Pancreatic cancer exhibits a high mortality rate resulting from metastasis and there is currently no effective treatment strategy. Hypoxia serves an important role in cancer cells, where cellular metabolic rate is high. The underlying mechanisms that trigger hypoxia and the invasion of pancreatic cancer cells remain unknown. Investigation of the importance of hypoxia in the invasion of pancreatic cancer cells for potential, novel treatment strategies is of primary concern. Cell Counting Kit‑8 assay, invasion assay, western blotting and reverse transcription‑quantitative polymerase chain reaction were used to investigate invasion and epithelial mesenchymal transition (EMT) and the expression of Notch1 in MiaPaCa2 cells treated with cobalt II chloride (CoCl2)...
January 26, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29391154/o-glcnacylation-affects-%C3%AE-catenin-and-e-cadherin-expression-cell-motility-and-tumorigenicity-of-colorectal-cancer
#15
Shani Ben Harosh-Davidovich, Isam Khalaila
O-GlcNAcylation, the addition of β-N-acetylglucosamine (O-GlcNAc) moiety to Ser/Thr residues, is a sensor of the cell metabolic state. Cancer diseases such as colon, lung and breast cancer, possess deregulated O-GlcNAcylation. Studies during the last decade revealed that O-GlcNAcylation is implicated in cancer tumorigenesis and proliferation. The Wnt/β-catenin signaling pathway and cadherin-mediated adhesion are also implicated in epithelial-mesenchymal transition (EMT), a key cellular process in invasion and cancer metastasis...
January 30, 2018: Experimental Cell Research
https://www.readbyqxmd.com/read/29367463/mutant-p53r270h-drives-altered-metabolism-and-increased-invasion-in-pancreatic-ductal-adenocarcinoma
#16
Heather K Schofield, Jörg Zeller, Carlos Espinoza, Christopher J Halbrook, Annachiara Del Vecchio, Brian Magnuson, Tania Fabo, Ayse Ece Cali Daylan, Ilya Kovalenko, Ho-Joon Lee, Wei Yan, Ying Feng, Saadia A Karim, Daniel M Kremer, Chandan Kumar-Sinha, Costas A Lyssiotis, Mats Ljungman, Jennifer P Morton, Stefanie Galbán, Eric R Fearon, Marina Pasca di Magliano
Pancreatic cancer is characterized by nearly universal activating mutations in KRAS. Among other somatic mutations, TP53 is mutated in more than 75% of human pancreatic tumors. Genetically engineered mice have proven instrumental in studies of the contribution of individual genes to carcinogenesis. Oncogenic Kras mutations occur early during pancreatic carcinogenesis and are considered an initiating event. In contrast, mutations in p53 occur later during tumor progression. In our model, we recapitulated the order of mutations of the human disease, with p53 mutation following expression of oncogenic Kras...
January 25, 2018: JCI Insight
https://www.readbyqxmd.com/read/29345287/intermittent-calorie-restriction-enhances-epithelial-mesenchymal-transition-through-the-alteration-of-energy-metabolism-in-a-mouse-tumor-model
#17
Osamu Kusuoka, Rina Fujiwara-Tani, Chie Nakashima, Kiyomu Fujii, Hitoshi Ohmori, Takuya Mori, Shingo Kishi, Yoshihiro Miyagawa, Kei Goto, Isao Kawahara, Hiroki Kuniyasu
The effect of intermittent calorie restriction (ICR) on cancer is controversial. In this study, we examined the effects of ICR and food content in syngeneic BALB/c mice injected with CT26 mouse colon cancer cells. Mice were subjected to 24-h fasting once a week for 4 weeks, and then provided with a control, high-calorie, or trans fatty acid-rich diet. While ICR resulted in increases in tumor weights, metastasis and in the number of cancer stem cells (CSCs) in the tumors or blood of mice fed the control and high-fat diets, it had no effect on body weight after 4 weeks...
February 2018: International Journal of Oncology
https://www.readbyqxmd.com/read/29343522/polyol-pathway-links-glucose-metabolism-to-the-aggressiveness-of-cancer-cells
#18
Annemarie Schwab, Aarif Siddiqui, Maria Eleni Vazakidou, Francesca Napoli, Martin Böttcher, Bianca Menchicchi, Umar Raza, Özge Saatci, Angela M Krebs, Fulvia Ferrazzi, Ida Rapa, Katja Dettmer-Wilde, Maximilian J Waldner, Arif B Ekici, Suhail Ahmed Kabeer Rasheed, Dimitrios Mougiakakos, Peter J Oefner, Özgür Şahin, Marco Volante, Florian R Greten, Thomas Brabletz, Paolo Ceppi
Cancer cells alter their metabolism to support their malignant properties. In this study, we report that the glucose-transforming polyol pathway (PP) gene aldo-keto-reductase-1-member-B1 (AKR1B1) strongly correlates with epithelial-to-mesenchymal transition (EMT). This association was confirmed in samples from lung cancer patients and from an EMT-driven colon cancer mouse model with p53 deletion. In vitro, mesenchymal-like cancer cells showed increased AKR1B1 levels, and AKR1B1 knockdown was sufficient to revert EMT...
January 17, 2018: Cancer Research
https://www.readbyqxmd.com/read/29331423/thymidylate-synthase-prompts-metastatic-progression-through-the-dtmp-associated-emt-process-in-pancreatic-ductal-adenocarcinoma
#19
Muxing Kang, Wen Zheng, Qing Chen, Wenjie Qin, Pengping Li, Shifei Huang, Yizhao Zhou, Lantian Wang, Haolei Cai, Wenjie Lu, Biao Jiang, Qingqu Guo, Jian Chen, Dylan Wan, Jianyu Rao, Yulian Wu
As a fundamental metabolic enzyme, anti-Thymidylate synthase (TS) strategy has been shown to be an effective therapy for human cancers. However, the genuine effects of TS in pancreatic ductal adenocarcinoma (PDA) are still conflicting. We systemically assessed the prognostic value and whether TS associated with malignant progression in PDA. Protein and mRNA expression level of TS were evaluated in en bloc PDA samples, the prognostic effect of TS expressed in cytoplasm or cytonuclear was determined separately in the first time...
April 10, 2018: Cancer Letters
https://www.readbyqxmd.com/read/29331414/inhibition-of-fasn-and-er%C3%AE-signalling-during-hyperglycaemia-induced-matrix-specific-emt-promotes-breast-cancer-cell-invasion-via-a-caveolin-1-dependent-mechanism
#20
H A Zielinska, J M P Holly, A Bahl, C M Perks
Since disturbed metabolic conditions such as obesity and diabetes can be critical determinants of breast cancer progression and therapeutic failure, we aimed to determine the mechanism responsible for their pro-oncogenic effects. Using non-invasive, epithelial-like ERα-positive MCF-7 and T47D human breast cancer cells we found that hyperglycaemia induced epithelial to mesenchymal transition (EMT), a key programme responsible for the development of metastatic disease. This was demonstrated by loss of the epithelial marker E-cadherin together with increases in mesenchymal markers such as vimentin, fibronectin and the transcription factor SLUG, together with an enhancement of cell growth and invasion...
April 10, 2018: Cancer Letters
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