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Author :
Publisher :
ISBN 13 : 9789175498096
Total Pages : 40 pages
Book Rating : 4.4/5 (98 download)
Download or read book Induction of Epithelial-mesenchymal Transition (EMT) in Women's Cancer written by and published by . This book was released on 2015 with total page 40 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Author : Joëlle Roche
Publisher : MDPI
ISBN 13 : 3038427934
Total Pages : 261 pages
Book Rating : 4.0/5 (384 download)
Download or read book The Epithelial-to-Mesenchymal Transition (EMT) in Cancer written by Joëlle Roche and published by MDPI. This book was released on 2018-04-09 with total page 261 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book is a printed edition of the Special Issue "The Epithelial-to-Mesenchymal Transition (EMT) in Cancer" that was published in Cancers
Author : Mohit Kumar Jolly
Publisher : MDPI
ISBN 13 : 3039367242
Total Pages : 512 pages
Book Rating : 4.0/5 (393 download)
Download or read book Epithelial-Mesenchymal Plasticity in Cancer Metastasis written by Mohit Kumar Jolly and published by MDPI. This book was released on 2020-12-29 with total page 512 pages. Available in PDF, EPUB and Kindle. Book excerpt: Recent studies have highlighted that epithelial-mesenchymal transition (EMT) is not only about cell migration and invasion, but it can also govern many other important elements such as immunosuppression, metabolic reprogramming, senescence-associated secretory phenotype (SASP), stem cell properties, therapy resistance, and tumor microenvironment interactions. With the on-going debate about the requirement of EMT for cancer metastasis, an emerging focus on intermediate states of EMT and its reverse process mesenchymal-epithelial transition (MET) offer new ideas for metastatic requirements and the dynamics of EMT/MET during the entire metastatic cascade. Therefore, we would like to initiate discussions on viewing EMT and its downstream signaling networks as a fulcrum of cellular plasticity, and a facilitator of the adaptive responses of cancer cells to distant organ microenvironments and various therapeutic assaults. We hereby invite scientists who have prominently contributed to this field, and whose valuable insights have led to the appreciation of epithelial-mesenchymal plasticity as a more comprehensive mediator of the adaptive response of cancer cells, with huge implications in metastasis, drug resistance, tumor relapse, and patient survival.
Author : Tao Sun
Publisher : Frontiers Media SA
ISBN 13 : 2832516343
Total Pages : 120 pages
Book Rating : 4.8/5 (325 download)
Download or read book Epithelial-Mesenchymal Transition (EMT) as a Therapeutic Target in Cancer written by Tao Sun and published by Frontiers Media SA. This book was released on 2023-03-03 with total page 120 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Author : Janine Marie Buonato
Publisher :
ISBN 13 :
Total Pages : 256 pages
Book Rating : 4.:/5 (952 download)
Download or read book Cell Signaling Regulatory Mechanisms Controlling Epithelial-mesenchymal Transition in Carcinoma written by Janine Marie Buonato and published by . This book was released on 2015 with total page 256 pages. Available in PDF, EPUB and Kindle. Book excerpt: Epithelial-mesenchymal transition (EMT) is a cellular program normally engaged during development and wound healing that is hijacked in many cancers to drive metastasis and resistance to therapy. The clinical implications of EMT in cancer progression have driven efforts to understand the cellular processes controlling EMT induction. Transforming growth factor-beta (TGF [beta]) and expression of related transcription factors potentiate EMT induction through complex and incompletely understood mechanisms. In this thesis, we investigated specific intracellular signaling pathways controlling maintenance of mesenchymal characteristics and EMT induction in response to growth factors in lung and pancreatic carcinoma cells. In lung carcinoma cells, extracellular signal-regulated kinase-1/2 (ERK1/2) pathway activation, which promotes cell survival and proliferation, was required for complete EMT induction. Furthermore, chronic ERK1/2 inhibition reversed baseline mesenchymal traits while simultaneously augmenting cellular sensitivity to a clinically approved small molecule EGFR inhibitor in cell lines with multiple clinically relevant modes of therapy resistance. In both lung and pancreatic carcinoma cell lines, TGF-mediated EMT was enhanced by co-treatment with epidermal growth factor (EGF), as had been noted in other contexts. We demonstrated that the ability of EGF to enhance TGF [beta]-mediated EMT depended on SH2 domain-containing phosphatase-2 (SHP2) activation through tyrosine phosphorylated adapter binding, which is required for complete ERK1/2 activation. Though SHP2 was not directly engaged and activated by TGF [beta], SHP2 was required for TGF [beta]-mediated effects. Incomplete or transient effects of ERK inhibition and SHP2 depletion motivated subsequent systematic evaluation of cell signaling processes engaged during EMT induction to identify other pathways that control mesenchymal dedifferentiation in pancreatic carcinoma cells. We thus developed a data-driven computational model to predict the relationships between multivariate signaling events and EMT-associated phenotypes in response to combinations of TGF [beta], EGF, and hepatocyte growth factor (HGF). Signaling intermediates that co-varied most with mesenchymal traits provided novel potential targets to inhibit EMT phenotype acquisition or restore epithelial traits in carcinoma. Together, this thesis enhanced mechanistic understanding of EMT regulation by SHP2, identified novel strategies to reverse EMT phenotypes in carcinoma cells, and generated a quantitative model to understand mesenchymal dedifferentiation, which can be leveraged in the future to improve clinical outcomes for cancer patients.
Author : Yuvabharath Kondaveeti
Publisher :
ISBN 13 :
Total Pages : 216 pages
Book Rating : 4.:/5 (959 download)
Download or read book Epithelial-mesenchymal Transition and Metabolic Reprogramming in Human Breast Cancer Cells written by Yuvabharath Kondaveeti and published by . This book was released on 2015 with total page 216 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Author : Pierre Savagner
Publisher : Springer Science & Business Media
ISBN 13 : 0387286713
Total Pages : 341 pages
Book Rating : 4.3/5 (872 download)
Download or read book Rise and Fall of Epithelial Phenotype written by Pierre Savagner and published by Springer Science & Business Media. This book was released on 2007-07-05 with total page 341 pages. Available in PDF, EPUB and Kindle. Book excerpt: Epithelial phenotype is a dynamic stage of differentiation that can be modulated during several physiological or pathological events. The rapid conversion to a mesenchymal-like phenotype is called an epithelial-mesenchymal transition (EMT). The Rise and Fall of Epithelial Phenotype is the first book to comprehensively introduce the concept of EMT. The first part of this volume describes main examples and models and explains their physiological relevance. These examples include hydra morphogenesis, gastrulation in mouse, drosophila and sea urchin, as well as neural crest cell migration and heart morphogenesis in vertebrates. Part two reviews in detail, specific EMT molecular pathways covering extracellular induction, transduction and transcription response and modulation of cell-cell adhesion structures. It emphasizes new specific pathways with potential medical applications. EMTs can also be linked to pathological events such as wound healing and cancer progression, as detailed in this section of the book.
Author : Kazuwa Nakao
Publisher : Springer
ISBN 13 : 4431556516
Total Pages : 330 pages
Book Rating : 4.4/5 (315 download)
Download or read book Innovative Medicine written by Kazuwa Nakao and published by Springer. This book was released on 2015-10-13 with total page 330 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book is devoted to innovative medicine, comprising the proceedings of the Uehara Memorial Foundation Symposium 2014. It remains extremely rare for the findings of basic research to be developed into clinical applications, and it takes a long time for the process to be achieved. The task of advancing the development of basic research into clinical reality lies with translational science, yet the field seems to struggle to find a way to move forward. To create innovative medical technology, many steps need to be taken: development and analysis of optimal animal models of human diseases, elucidation of genomic and epidemiological data, and establishment of “proof of concept”. There is also considerable demand for progress in drug research, new surgical procedures, and new clinical devices and equipment. While the original research target may be rare diseases, it is also important to apply those findings more broadly to common diseases. The book covers a wide range of topics and is organized into three complementary parts. The first part is basic research for innovative medicine, the second is translational research for innovative medicine, and the third is new technology for innovative medicine. This book helps to understand innovative medicine and to make progress in its realization.
Author : Anupam Bishayee
Publisher : MDPI
ISBN 13 : 3038973106
Total Pages : 285 pages
Book Rating : 4.0/5 (389 download)
Download or read book Natural Products for Cancer Prevention and Therapy written by Anupam Bishayee and published by MDPI. This book was released on 2018-11-07 with total page 285 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book is a printed edition of the Special Issue "Natural Products for Cancer Prevention and Therapy" that was published in Nutrients
Author : Norman F. Cheville
Publisher : John Wiley & Sons
ISBN 13 : 0813803306
Total Pages : 997 pages
Book Rating : 4.8/5 (138 download)
Download or read book Ultrastructural Pathology written by Norman F. Cheville and published by John Wiley & Sons. This book was released on 2009-06-30 with total page 997 pages. Available in PDF, EPUB and Kindle. Book excerpt: Ultrastructural Pathology
Author : Görkem Eskiizmir
Publisher :
ISBN 13 :
Total Pages : pages
Book Rating : 4.:/5 (115 download)
Download or read book Epithelial-Mesenchymal Transition in Tumor Microenvironment Induced by Hypoxia written by Görkem Eskiizmir and published by . This book was released on 2018 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: A tumor microenvironment contains various noncancerous cells including adipocytes, fibroblasts, immune and inflammatory cells, neuroendocrine cells, pericytes, vascular and lymphatic endothelial cells, and the extracellular matrix that surrounds cancerous cells. In the tumor microenvironment, cancer cells interact and cross talk with noncancerous cells and orchestrate different mechanisms of cancer such as tumorigenesis, angiogenesis, and metastasis. Moreover, the expansive nature of cancer cells and chaotic angiogenesis affect microcirculation as well as alter the oxygen concentration progressively. Hypoxia, a key player in the multistep process of cancer metastasis, is important in different regions of the tumor microenvironment. Hypoxia may transform cancer cells to become more aggressive and invasive by triggering overexpression of several hypoxia-related factors that activate epithelial-mesenchymal transition (EMT). Herein, the current knowledge of how hypoxia-driven EMT is presented in the tumor microenvironment of solid cancers is discussed.
Author : Chih-Chien Chou
Publisher :
ISBN 13 :
Total Pages : pages
Book Rating : 4.:/5 (922 download)
Download or read book Inhibition of Epithelial-to-mesenchymal Transition by Anti-tumor Agents in Cancer Cells written by Chih-Chien Chou and published by . This book was released on 2014 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Epithelial-mesenchymal transition (EMT) is a critical process that confers to cancer cells the ability to invade basement membranes and metastasize to distant sites. Here, we report a novel function of the metabolic sensor adenosine monophosphate-activated protein kinase (AMPK) in suppressing EMT by modulating the Akt-MDM2-Foxo3 signaling axis. This mechanistic link was supported by the effects of siRNA-mediated knockdown and pharmacological activation of AMPK on epithelial (E-cadherin) and mesenchymal markers (vimentin, YB-1, Snail) in a panel of breast and prostate cancer cell lines. Exposure of cells to OSU-53, a novel allosteric AMPK activator, as well as metformin and AICAR, reversed their mesenchymal phenotype, which could be abrogated by AMPK silencing. This phenotypic change was mediated through Foxo3a activation as knockdown and ectopic expression of Foxo3a mimicked the effects of AMPK silencing and OSU-53-induced activation on these EMT markers, respectively. Mechanistically, Foxo3a activation led to the transactivation of the E-cadherin gene and repression of genes encoding EMT-inducing transcription factors. Evidence indicates that OSU-53 activated Foxo3a through two Akt-dependent pathways: nuclear localization by blocking Akt- and IKK-mediated phosphorylation, and protein stabilization by cytoplasmic sequestration of MDM2, an E3 ligase responsible for Foxo3a degradation. This mode of activation contrasts with a previously reported in which AMPK increased Foxo3a transcriptional activity through direct phosphorylation without affecting its subcellular localization. Functionally, the suppressive effect of OSU-53 on EMT was demonstrated by its ability to block the invasive phenotypes of MDA-MB-231 and PC-3 cells in vitro and lung metastasis in the 4T1 orthotopic mammary cancer model.
Author : Joëlle Roche (Ed.)
Publisher :
ISBN 13 :
Total Pages : 254 pages
Book Rating : 4.:/5 (113 download)
Download or read book The Epithelial-to-Mesenchymal Transition (EMT) in Cancer written by Joëlle Roche (Ed.) and published by . This book was released on 2018 with total page 254 pages. Available in PDF, EPUB and Kindle. Book excerpt: The epithelial-to-mesenchymal transition (EMT) is a highly dynamic process with multiple transitional states, by which epithelial cells can convert into a mesenchymal phenotype. This process involves loss of cellular adhesion and cellular polarity, and an improvement in migratory and invasive properties. It occurs during normal embryonic development, tissue regeneration, organ fibrosis, and wound healing. It is also involved in tumor progression with metastatic expansion, and plays a major role in resistance to cancer treatment. In cancers, EMT inducers are hypoxia, cytokines and growth factors secreted by the tumor microenvironment, stroma crosstalk, metabolic changes, innate and adaptive immune responses, and treatment with antitumor drugs. Switch in gene expression from epithelial to mesenchymal phenotype is triggered by complex regulatory networks involving transcriptional control, non-coding RNAs, chromatin remodeling and epigenetic modifications, alternative splicing, post-translational regulation, protein stability and subcellular localization. Reversion of EMT, the mesenchymal-to-epithelial transition (MET), affects circulating cancer cells when they reach a desirable metastatic niche to develop secondary tumors. More knowledge and control of EMT to MET is necessary and will be beneficial for patients for cancer treatment. This current Special Issue entitled "Epithelial to Mesenchymal Transition in Cancer" will address these questions.
Author : Toshio Nakanishi
Publisher : Springer Nature
ISBN 13 : 9811511853
Total Pages : 374 pages
Book Rating : 4.8/5 (115 download)
Download or read book Molecular Mechanism of Congenital Heart Disease and Pulmonary Hypertension written by Toshio Nakanishi and published by Springer Nature. This book was released on 2020-02-28 with total page 374 pages. Available in PDF, EPUB and Kindle. Book excerpt: This open access book focuses on the molecular mechanism of congenital heart disease and pulmonary hypertension, offering new insights into the development of pulmonary circulation and the ductus arteriosus. It describes in detail the molecular mechanisms involved in the development and morphogenesis of the heart, lungs and ductus arteriosus, covering a range of topics such as gene functions, growth factors, transcription factors and cellular interactions, as well as stem cell engineering technologies. The book also presents recent advances in our understanding of the molecular mechanism of lung development, pulmonary hypertension and molecular regulation of the ductus arteriosus. As such, it is an ideal resource for physicians, scientists and investigators interested in the latest findings on the origins of congenital heart disease and potential future therapies involving pulmonary circulation/hypertension and the ductus arteriosus.
Author : Alexandra H Besser
Publisher :
ISBN 13 :
Total Pages : pages
Book Rating : 4.:/5 (12 download)
Download or read book P27 Drives PI3K-dependent Cancer Metastasis by Activating EMT Transcription Factors to Induce an EMT Program written by Alexandra H Besser and published by . This book was released on 2015 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: In normal cells, p27 regulates cell cycle and functions as an atypical tumor suppressor. Unlike typical tumor suppressors such as p16 and pRb, p27 gene deletions or mutations are rarely observed in human cancers. Instead, p27 is deregulated through either excess degradation or through key C-terminal phosphorylations, in human cancers. Phosphorylation at T157 or T198 by different PI3K effector kinases allows p27 to take on new binding partners and promote oncogenic transformation. This thesis addresses the functional contribution of T157 and T198-phosphorylated, deregulated p27 to cancer progression and metastasis. By studying the effects of a transfected cell cycle defective (CK-) and double phosphomimetic p27 mutant (T157D/T198D) in transformed and non-transformed cells, we found that phosphorylation of p27 at T157 or T198 by PI3K/mTOR directly regulates tumor cell migration and invasion. Targeted inhibition of PI3K/mTOR impairs tumor cell motility and metastasis via modulation of p27. Furthermore, we uncovered a novel oncogenic function of p27 to promote tumor progression. p27CK-DD induced epithelial-mesenchymal transition (EMT) and transformation of human mammary epithelial cells and enhanced the mesenchymal characteristics and metastatic potential of breast cancer cell lines. Knockdown of p27 in highly metastatic EMT-transformed cell lines with enriched p27pT157pT198 (p27pTpT) reverted EMT and impaired metastatic potential. Mechanistically, we showed phosphorylation of p27 at T157 and T198 promotes the activation and induction of several EMT drivers and transcription factors to induce EMT. p27CK-DD activates STAT3 and facilitates its transactivation of TWIST1 to induce EMT. Pharmacological inhibition of STAT3 or dominant negative STAT3 (STAT3DN) decreased TWIST1 expression and reversed p27CK-DD-mediated EMT and tumor progression, while constitutively active STAT3 (STAT3CA) rescued the EMT phenotype and metastatic potential in p27 knockdown cells. We also identified a potential signaling feed-forward loop containing AKT activation, p27 phosphorylation, STAT3 activation and further AKT activation that might contribute to tumor progression. This thesis work also provides novel evidence for p27 as a transcriptional co- regulator of c-Jun. We prove evidence that C-terminally phophorylated p27 binds and activates c-Jun, and forms a complex with c-Jun at an enhancer region upstream of the TGF-B2 gene to upregulate TGF-B2. Not only does p27pTpT upregulate expression of the ligand, TGF-?2, p27pTpT is required for maximal TGF-B2-stimulated SMAD3 activation, SNAI1 induction, and matrigel invasion. Following addition of exogenous TGF-B2 ligand, p27 forms a tripartite complex with c-Jun and SMAD3 on the SNAI1 promoter, thus revealing an additional mechanism by which PI3K-activated, C-terminally phosphorylated p27 drives EMT and metastasis. These findings reveal a novel, oncogenic function of p27 to promote tumor progression through EMT via STAT3-mediated induction of TWIST1, c-Jun-mediated TGF-B2 induction, and c-Jun/SMAD3-mediated SNAI1 induction. Combined inhibition of AKT, STAT3, and TGF-B2 in PI3K/mTOR activated, p27pTpT enriched human cancers may ultimately have therapeutic potential to limit p27-mediated EMT and cancer metastasis.
Author : Raul Fleischmajer (ed)
Publisher :
ISBN 13 :
Total Pages : 348 pages
Book Rating : 4.3/5 (91 download)
Download or read book Epithelial-mesanchymal Interactions written by Raul Fleischmajer (ed) and published by . This book was released on 1968 with total page 348 pages. Available in PDF, EPUB and Kindle. Book excerpt:
Author : Andrew Thomas Chang
Publisher :
ISBN 13 : 9781267434708
Total Pages : 89 pages
Book Rating : 4.4/5 (347 download)
Download or read book Dissecting the Molecular Mechanism of Epithelial-to-mesenchymal Transition in Development and in Twist-driven Tumor Metastasis written by Andrew Thomas Chang and published by . This book was released on 2012 with total page 89 pages. Available in PDF, EPUB and Kindle. Book excerpt: Epithelial-to-mesenchymal transition (EMT) is a highly conserved cellular process through which polarized and stationary epithelial cells become highly motile mesenchymal cells. EMT is an essential cellular process during embryogenesis, such as mesoderm induction, and more recently has been shown to be an important step in cancer metastasis. In both cases, epithelial cells must break away from neighboring cells and migrate to a distant location. Even though EMT has an important role in development and pathogenesis, the molecular machinery that drives EMT in mesoderm development and cancer metastasis is far from being fully understood. Therefore, for my dissertation, I sought to characterize the mechanism of EMT in both processes to gain a better understanding of cell migration and morphogenesis. Twist is a known inducer of EMT and tumor invasion and metastasis. To understand how Twist regulates target gene expression, we applied chromatin immuno-precipitation coupled with high-throughput sequencing to characterize its genome-wide DNA binding patterns. Using this approach, we found that through cooperative binding, Twist recognizes an evolutionarily conserved double E-box motif to regulate transcription of target genes. Furthermore, we show that the highly conserved WR domain of Twist mediates the high affinity cooperative binding of Twist to the double E-box motif. Functionally, the WR domain is essential for the ability of Twist to promote EMT. To characterize EMT in mammalian mesoderm formation, we utilized the in vitro embryoid body model system that forms all three germ layers during differentiation. After establishing the embryoid body system as an effective ex vivo model to study mesoderm formation, I first characterized the expression profile of known EMT-inducing transcription factors during mesoderm development. By knocking down individual genes using shRNA, I identified several EMT transcription factors to be essential for mesoderm formation and began to elucidate how a group of EMT-inducing transcription factors function together to orchestrate mesoderm formation. By studying the molecular mechanism of EMT in development and cancer metastasis, we have gained a better understanding of EMT as an essential cellular process and as a possible therapeutic target to inhibit cancer progression.
