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Cellular reprograming

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https://www.readbyqxmd.com/read/28213718/reprogramming-cell-fates-by-small-molecules
#1
REVIEW
Xiaojie Ma, Linghao Kong, Saiyong Zhu
Reprogramming cell fates towards pluripotent stem cells and other cell types has revolutionized our understanding of cellular plasticity. During the last decade, transcription factors and microRNAs have become powerful reprogramming factors for modulating cell fates. Recently, many efforts are focused on reprogramming cell fates by non-viral and non-integrating chemical approaches. Small molecules not only are useful in generating desired cell types in vitro for various applications, such as disease modeling and cell-based transplantation, but also hold great promise to be further developed as drugs to stimulate patients' endogenous cells to repair and regenerate in vivo...
February 17, 2017: Protein & Cell
https://www.readbyqxmd.com/read/28210259/resolution-of-cancer-promoting-inflammation-a-new-approach-for-anticancer-therapy
#2
REVIEW
Qi Zhang, Bo Zhu, Yongsheng Li
Inflammation is a protective response that eliminates harmful stimuli and restores tissue homeostasis, whereas the failure to resolve inflammation leads to the development of malignancies. Immune cells in the tumor inflammatory microenvironment endow cancer cells with their specific hallmarks, including mutations, metabolic reprograming, angiogenesis, invasion, and metastasis. Targeting the inflammatory microenvironment with anti-inflammatory drugs (e.g., aspirin) or by enhancing antitumor immunity (e.g., chimeric antigen receptor T cell therapy) has been extensively investigated and has achieved promising results in many cancers...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28202510/myc-mediates-large-oncosome-induced-fibroblast-reprogramming-in-prostate-cancer
#3
Valentina R Minciacchi, Cristiana Spinelli, Mariana Reis-Sobreiro, Lorenzo Cavallini, Sungyong You, Mandana Zandian, Xiaohong Li, Paola Chiarugi, Rosalyn M Adam, Edwin M Posadas, Giuseppe Viglietto, Michael R Freeman, Emanuele Cocucci, Neil A Bhowmick, Dolores Di Vizio
Communication between cancer cells and the tumor microenvironment results in the modulation of complex signaling networks that facilitate tumor progression. Here we describe a new mechanism of intercellular communication originating from large oncosomes (LO), which are cancer cell-derived, atypically large (1-10 μm) extracellular vesicles (EV). We demonstrate that, in the context of prostate cancer, LO harbor sustained AKT1 kinase activity, nominating them as active signaling platforms. Active AKT1 was detected in circulating EV from the plasma of metastatic prostate cancer patients and was LO specific...
February 15, 2017: Cancer Research
https://www.readbyqxmd.com/read/28202507/yap-taz-mediated-upregulation-of-gab2-leads-to-increased-sensitivity-to-growth-factor-induced-activation-of-the-pi3k-pathway
#4
Chao Wang, Chao Gu, Kang Jin Jeong, Dong Zhang, Wei Guo, Yiling Lu, Zhenlin Ju, Nattapon Panupinthu, Ji Yeon Yang, Mihai Gagea, Patrick Kwok Shing Ng, Fan Zhang, Gordon B Mills
The transcription regulators YAP and TAZ function as effectors of the HIPPO signaling cascade, critical for organismal development, cell growth, and cellular reprogramming, and YAP/TAZ is commonly misregulated in human cancers. The precise mechanism by which aberrant YAP/TAZ promotes tumor growth remains unclear. The HIPPO tumor suppressor pathway phosphorylates YAP and TAZ resulting in cytosolic sequestration with subsequent degradation. Here we report that the phosphatidylinositol 3' kinase (PI3K)/AKT pathway, which is critically involved in the pathophysiology of endometrial cancer (EC), interacts with the HIPPO pathway at multiple levels...
February 15, 2017: Cancer Research
https://www.readbyqxmd.com/read/28202352/amino-acid-transporter-slc38a3-promotes-metastasis-of-non-small-cell-lung-cancer-cells-by-activating-pdk1
#5
Yanhui Wang, Li Fu, Minqing Cui, Yongbin Wang, Yan Xu, Molin Li, Jun Mi
BACKGROUND: Tumor metastasis is a finely-tuned pathological process coupled to metabolic reprogramming that includes both glutamine and glucose. The solute carrier SLC38A3, a member of amino acid/polyamine/organocation (APC) superfamily, is an L-glutamine transporter. It is not clear whether SLC38A3 involves the metastasis of NSCLC (non small cell lung cancer). METHODS: The scratch test and transwell assay were used to determine the ability of NSCLC to migrate. Cellular amino acids content was determined by mass spectrometry...
February 12, 2017: Cancer Letters
https://www.readbyqxmd.com/read/28199202/racial-disparity-in-metabolic-regulation-of-cancer
#6
Kuldeep S Attri, Divya Murthy, Pankaj K Singh
Genetic mutations and metabolic reprogramming are two key hallmarks of cancer, required for proliferation, invasion, and metastasis of the disease. While genetic mutations, whether inherited or acquired, are critical for the initiation of tumor development, metabolic reprogramming is an effector mechanism imperative for adaptational transition during the progression of cancer. Recent findings in the literature emphasize the significance of molecular cross-talk between these two cellular processes in regulating signaling and differentiation of cancer cells...
March 1, 2017: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/28198437/increased-nutrient-availability-in-dense-breast-tissue-of-postmenopausal-women-in-vivo
#7
Annelie Abrahamsson, Anna Rzepecka, Charlotta Dabrosin
Metabolic reprogramming is a hallmark of cancer. Nutrient availability in the tissue microenvironment determines cellular events and may play a role in breast carcinogenesis. High mammographic density is an independent risk factor for breast cancer. Whether nutrient availability differs in normal breast tissues with various densities is unknown. Therefore we investigated whether breast tissues with various densities exhibited differences in nutrient availability. Healthy postmenopausal women from the regular mammographic screening program who had either predominantly fatty breast tissue (nondense), n = 18, or extremely dense breast tissue (dense), n = 20, were included...
February 15, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28197395/characterization-of-the-tumor-microenvironment-and-tumor-stroma-interaction-by-non-invasive-preclinical-imaging
#8
REVIEW
Nirilanto Ramamonjisoa, Ellen Ackerstaff
Tumors are often characterized by hypoxia, vascular abnormalities, low extracellular pH, increased interstitial fluid pressure, altered choline-phospholipid metabolism, and aerobic glycolysis (Warburg effect). The impact of these tumor characteristics has been investigated extensively in the context of tumor development, progression, and treatment response, resulting in a number of non-invasive imaging biomarkers. More recent evidence suggests that cancer cells undergo metabolic reprograming, beyond aerobic glycolysis, in the course of tumor development and progression...
2017: Frontiers in Oncology
https://www.readbyqxmd.com/read/28196802/metabolic-remodeling-during-the-loss-and-acquisition-of-pluripotency
#9
REVIEW
Julie Mathieu, Hannele Ruohola-Baker
Pluripotent cells from the early stages of embryonic development have the unlimited capacity to self-renew and undergo differentiation into all of the cell types of the adult organism. These properties are regulated by tightly controlled networks of gene expression, which in turn are governed by the availability of transcription factors and their interaction with the underlying epigenetic landscape. Recent data suggest that, perhaps unexpectedly, some key epigenetic marks, and thereby gene expression, are regulated by the levels of specific metabolites...
February 15, 2017: Development
https://www.readbyqxmd.com/read/28196665/complement-s-hidden-arsenal-new-insights-and-novel-functions-inside-the-cell
#10
M Kathryn Liszewski, Michelle Elvington, Hrishikesh S Kulkarni, John P Atkinson
A key component of both innate and adaptive immunity, new understandings of the complement system are expanding its roles beyond that traditionally appreciated. Evidence is accumulating that complement has an intracellular arsenal of components that provide not only immune defense, but also assist in key interactions for host cell functions. Although early work has primarily centered on T cells, the intracellular complement system likely functions in many if not most cells of the body. Some of these functions may trace their origins to the primitive complement system that began as a primeval form of C3 likely tasked for protection from intracellular pathogen invasion...
February 10, 2017: Molecular Immunology
https://www.readbyqxmd.com/read/28195240/mir302-regulates-snai1-expression-to-control-mesangial-cell-plasticity
#11
L De Chiara, D Andrews, A Watson, G Oliviero, G Cagney, J Crean
Cell fate decisions are controlled by the interplay of transcription factors and epigenetic modifiers, which together determine cellular identity. Here we elaborate on the role of miR302 in the regulation of cell plasticity. Overexpression of miR302 effected silencing of the TGFβ type II receptor and facilitated plasticity in a manner distinct from pluripotency, characterized by increased expression of Snail. miR302 overexpressing mesangial cells also exhibited enhanced expression of EZH2 coincident with Snail upregulation...
February 14, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28193997/stepwise-reprogramming-of-liver-cells-to-a-pancreas-progenitor-state-by-the-transcriptional-regulator-tgif2
#12
Nuria Cerdá-Esteban, Heike Naumann, Silvia Ruzittu, Nancy Mah, Igor M Pongrac, Corinna Cozzitorto, Angela Hommel, Miguel A Andrade-Navarro, Ezio Bonifacio, Francesca M Spagnoli
The development of a successful lineage reprogramming strategy of liver to pancreas holds promises for the treatment and potential cure of diabetes. The liver is an ideal tissue source for generating pancreatic cells, because of its close developmental origin with the pancreas and its regenerative ability. Yet, the molecular bases of hepatic and pancreatic cellular plasticity are still poorly understood. Here, we report that the TALE homeoprotein TGIF2 acts as a developmental regulator of the pancreas versus liver fate decision and is sufficient to elicit liver-to-pancreas fate conversion both ex vivo and in vivo...
February 13, 2017: Nature Communications
https://www.readbyqxmd.com/read/28192065/vascular-endothelial-growth-factor-a-and-leptin-expression-associated-with-ectopic-proliferation-and-retinal-dysplasia-in-zebrafish-optic-pathway-tumors
#13
Laura E Schultz, Staci L Solin, Wesley A Wierson, Janna M Lovan, Judith Syrkin-Nikolau, Deborah E Lincow, Andrew J Severin, Donald S Sakaguchi, Maura McGrail
In the central nervous system injury induces cellular reprogramming and progenitor proliferation, but the molecular mechanisms that limit regeneration and prevent tumorigenesis are not completely understood. We previously described a zebrafish optic pathway tumor model in which transgenic Tg(flk1:RFP)is18/+ adults develop nonmalignant retinal tumors. Key pathways driving injury-induced glial reprogramming and regeneration contributed to tumor formation. In this study, we examine a time course of proliferation and present new analyses of the Tg(flk1:RFP)is18/+ dysplastic retina and tumor transcriptomes...
February 13, 2017: Zebrafish
https://www.readbyqxmd.com/read/28191771/linking-pluripotency-reprogramming-and-cancer
#14
Juan Manuel Iglesias, Juan Gumuzio, Angel G Martin
Tumor development and the generation of induced pluripotent stem cells are highly comparable processes with striking similarities. Cellular plasticity is inherent to tumor evolution, rendering cells that acquire a stem cell-like phenotype, for which Sox2 activation has proved instrumental for the plastic acquisition of stemness properties in tumor cells. Understanding the molecular mechanisms underlying both events might uncover novel approaches for the development of anticancer therapeutics and constitute model systems for understanding tumor generation and ensuring the biosafety of cell-based therapies...
February 2017: Stem Cells Translational Medicine
https://www.readbyqxmd.com/read/28185461/-epithelial-mesenchymal-transition-in-tumor-tissue-and-its-role-for-metastatic-spread-of-cancer
#15
V M Matějka, J Fínek, M Králíčková
BACKGROUND: Metastasis, recurrence, and resistance to chemotherapy are leading causes of the majority of cancer-related mortality worldwide. The process of metastasis can be artificially divided into a series of sequential, highly organized, and organ-specific steps. The underlying mechanisms are still poorly understood, but are believed to be mediated by epithelial-mesenchymal transition (EMT). First described in embryogenesis, EMT is a cellular reprogramming process in which epithelial cells acquire a mesenchymal phenotype...
2017: Klinická Onkologie: Casopis Ceské a Slovenské Onkologické Spolecnosti
https://www.readbyqxmd.com/read/28185067/new-programmers-in-tissue-macrophage-activation
#16
REVIEW
Anna C Aschenbrenner, Joachim L Schultze
Tissue macrophages and monocyte-derived macrophages are under continuous influence from environmental signals that define their activation status. Along these lines, macrophages integrate tissue and stress signals and are specifically programmed by these signals towards a spectrum of functions necessary to fulfill their duty within their particular microenvironment, be it homeostatic tissue function, response to inflammatory pathophysiology, or even resolution of an inflammation. Recent years have seen tremendous progress in our understanding how macrophages at different sites are transcriptionally and epigenetically programmed to execute their diverse tasks throughout the body...
February 9, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/28184935/involvement-of-ezh2-in-aerobic-glycolysis-of-prostate-cancer-through-mir-181b-hk2-axis
#17
Tao Tao, Ming Chen, Ranran Jiang, Han Guan, Yeqing Huang, Huan Su, Qiang Hu, Xu Han, Jun Xiao
Recent studies suggest that several types of tumors preferentially metabolize glucose through aerobic glycolysis, a phenomenon known as the Warburg effect. However, it remains largely unexplored whether metabolic reprogramming is involved in prostate cancer (PCa) progression. In this study, we found that histone methyltransferase enhancer of zeste homolog 2 (EZH2) dysregulated in PCa development regulated cellular growth and aerobic glycolysis through miR-181b/hexokinase 2 (HK2) axis. Aberrant expression profiles of coding RNA and microRNA were examined by two large, independent clinical prostate cancer data sets...
March 2017: Oncology Reports
https://www.readbyqxmd.com/read/28183803/hexokinase-ii-derived-cell-penetrating-peptide-targets-mitochondria-and-triggers-apoptosis-in-cancer-cells
#18
Abiy D Woldetsadik, Maria C Vogel, Wael M Rabeh, Mazin Magzoub
Overexpression of mitochondria-bound hexokinase II (HKII) in cancer cells plays an important role in their metabolic reprogramming and protects them against apoptosis, thereby facilitating their growth and proliferation. Here, we show that covalently coupling a peptide that corresponds to the mitochondrial membrane-binding N-terminal domain of HKII (pHK) to a short, penetration-accelerating sequence (PAS) enhances the cellular uptake, mitochondrial localization, and cytotoxicity of the peptide in HeLa cells...
February 9, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28183717/the-transcriptional-regulator-of-the-chaperone-response-hsf1-controls-hepatic-bioenergetics-and-protein-homeostasis
#19
Aijun Qiao, Xiongjie Jin, Junfeng Pang, Demetrius Moskophidis, Nahid F Mivechi
Metabolic energy reprogramming facilitates adaptations to a variety of stress conditions and cellular dysfunction, but how the energetic demands are monitored and met in response to physiological stimuli remains elusive. Our data support a model demonstrating that heat shock factor 1 (HSF1), a master transcriptional regulator of the chaperone response, has been coopted from its role as a critical protein quality-control regulator to having a central role in systemic energy sensing and for metabolic adaptation to nutrient availability...
February 9, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28178232/synthetic-vulnerabilities-of-mesenchymal-subpopulations-in-pancreatic-cancer
#20
Giannicola Genovese, Alessandro Carugo, James Tepper, Frederick Scott Robinson, Liren Li, Maria Svelto, Luigi Nezi, Denise Corti, Rosalba Minelli, Piergiorgio Pettazzoni, Tony Gutschner, Chia-Chin Wu, Sahil Seth, Kadir Caner Akdemir, Elisabetta Leo, Samirkumar Amin, Marco Dal Molin, Haoqiang Ying, Lawrence N Kwong, Simona Colla, Koichi Takahashi, Papia Ghosh, Virginia Giuliani, Florian Muller, Prasenjit Dey, Shan Jiang, Jill Garvey, Chang-Gong Liu, Jianhua Zhang, Timothy P Heffernan, Carlo Toniatti, Jason B Fleming, Michael G Goggins, Laura D Wood, Alessandro Sgambato, Abbas Agaimy, Anirban Maitra, Charles W M Roberts, Huamin Wang, Andrea Viale, Ronald A DePinho, Giulio F Draetta, Lynda Chin
Malignant neoplasms evolve in response to changes in oncogenic signalling. Cancer cell plasticity in response to evolutionary pressures is fundamental to tumour progression and the development of therapeutic resistance. Here we determine the molecular and cellular mechanisms of cancer cell plasticity in a conditional oncogenic Kras mouse model of pancreatic ductal adenocarcinoma (PDAC), a malignancy that displays considerable phenotypic diversity and morphological heterogeneity. In this model, stochastic extinction of oncogenic Kras signalling and emergence of Kras-independent escaper populations (cells that acquire oncogenic properties) are associated with de-differentiation and aggressive biological behaviour...
February 16, 2017: Nature
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