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Molecular mechanisms of epithelial mesenchymal transition

Molecular mechanisms of epithelial-mesenchymal transition

  1. Molecular mechanisms of epithelial-mesenchymal transition Key Points. The epithelial-mesenchymal transition (EMT) process results in the downregulation of epithelial, and... Abstract. The transdifferentiation of epithelial cells into motile mesenchymal cells, a process known as... Main. The idea.
  2. g growth factor-β (TGF-β), are known to induce EMT and metastases in breast, lung, colorectal, and other cancers. Several downstream targets of the ERK5 pathway, such as myocyte-specific enhancer factor 2c (MEF2C), activator protein-1 (AP-1.
  3. Molecular mechanisms of epithelial to mesenchymal transition in tumor metastasis. Epithelial to mesenchymal transition (EMT) is a process during which cancer cells lose epithelial features, cytoskeletal architecture is re-organized, cell shape changes and cells activate genes that help to define mesenchymal phenotype, what leads to an increased.
  4. The transdifferentiation of epithelial cells into motile mesenchymal cells, a process known as epithelial-mesenchymal transition (EMT), is integral in development, wound healing and stem cell behaviour, and contributes pathologically to fibrosis and cancer progression. This switch in cell differentiation and behaviour is mediated by key transcription factors, including SNAIL, zinc-finger E-box-binding (ZEB) and basic helix-loop-helix transcription factors, the functions of which.
  5. The transdifferentiation of epithelial cells into motile mesenchymal cells, a process known as epithelial-mesenchymal transition (EMT), is integral in development, wound healing and stem cell behaviour, and contributes pathologically to fibrosis and cancer progression
  6. Epithelial-mesenchymal transition (EMT) is integral to development and pathology. This switch in cell differentiation and behaviour requires key transcription factors, including SNAIL, zinc.
  7. The morphological and molecular mechanisms of epithelial/endothelial-to-mesenchymal transition and its involvement in atherosclerosis Cell transdifferentiation occurs during cardiovascular development or remodeling either as a pathologic feature in the progression of disease or as a response to injury

The Molecular Mechanism of Epithelial-Mesenchymal Transition for BreastCarcinogenesis. Li CJ(1)(2), Chu PY(3)(4)(5), Yiang GT(6)(7), Wu MY(8)(9). Author information: (1)Department of Obstetrics and Gynecology, Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan Melanoma is a malignant cutaneous cancer of high metastasis and lethal rates. Epithelial-mesenchymal transition (EMT) plays an important role in the embryonic developmental process that is often activated during tumorigenesis and metastasis The morphological and molecular mechanisms of epithelial/endothelial-to-mesenchymal transition and its involvement in atherosclerosis 1. Introduction. In the past decades, the discovery of non-myeloid stem cells and their ability to differentiate into... 2. EndMT a form of EMT. The morphological and.

Molecular Mechanisms of Epithelial to Mesenchymal Transition Regulated by ERK5 Signaling Akshita B. Bhatt 1 , Saloni Patel 2 , Margarite D. Matossian 3 , Deniz A. Ucar 4 , Lucio Miele 4 , Matthew E. Burow 3 Cancer metastasis consists of a sequential series of events, and the epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) are recognized as critical events for metastasis of carcinomas. A current area of focus is the histopathological similarity between primary and metastatic tumors, and MET at sites of metastases has been postulated to be part of the process of metastatic tumor formation. Here, we summarize accumulating evidence from.

Molecular Mechanisms of Epithelial to Mesenchymal

Epithelial-mesenchymal transition (EMT) is a reversible cellular programme that transiently places epithelial cells into quasi-mesenchymal cell states 1, 2, 3, 4. During this process, epithelial.. Epithelial-mesenchymal transition (EMT), a pivotal step in cancer progression, is a phenotypic switch that permanently or transiently converts epithelial cells into mesenchymal-like cells Epithelial to mesenchymal transition (EMT) is a process during which cancer cells lose epithelial features, cytoskeletal architecture is re-organized, cell shape changes and cells activate genes that help to define mesenchymal phenotype, what leads to an increased cell motility and dissemination of tumor to distant metastatic sites Epithelial-mesenchymal transition and drug resistance: role, molecular mechanisms, and therapeutic strategies. Sui H (1), Zhu L, Deng W, Li Q. (1)Department of Medical Oncology, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China. Chemotherapy is an important therapeutic option for most cancer patients; however,.

The transforming growth factor-β (TGF-β) signaling pathway plays multiple regulatory roles in the tumorigenesis and development of cancer. TGF-β can inhibit the growth and proliferation of epithelial cells and induce apoptosis, thereby playing a role in inhibiting breast cancer. Therefore, the loss of response in epithelial cells that leads to the inhibition of cell proliferation due to TGF. The epithelial-mesenchymal transition is a process by which epithelial cells lose their cell polarity and cell-cell adhesion, and gain migratory and invasive properties to become mesenchymal stem cells; these are multipotent stromal cells that can differentiate into a variety of cell types. EMT is essential for numerous developmental processes including mesoderm formation and neural tube formation. EMT has also been shown to occur in wound healing, in organ fibrosis and in the.

Molecular mechanisms of epithelial to mesenchymal

Several molecular mechanisms contribute directly and mechanically to the loss of epithelial phenotype. During epithelial-mesenchymal transition (EMT), adherens junctions and desmosomes are at least partially dissociated The roles of HLH transcription factors in epithelial mesenchymal transition and multiple molecular mechanisms. Teng Y(1), Li X. Author information: (1)Center for Translational Medicine, The First Affiliated Hospital, School of Medicine, Xi'an Jiaotong University, Xi'an, 710061, People's Republic of China, navimoon@126.com. Epithelial-to-mesenchymal transition (EMT) is presently recognized as. Epithelial-mesenchymal transition (EMT) is defined by the loss of epithelial characteristics and the acquisition of a mesenchymal phenotype. In this process, cells acquire molecular alterations that facilitate dysfunctional cell-cell adhesive interactions and junctions. These processes may promote cancer cell progression and invasion into the surrounding microenvironment. Such. The epithelial-mesenchymal transition (EMT) provides a strong driving force in the progression of various human cancers and the development of chemoresistance. Recently, numbers of studies have demonstrated that microRNAs (miRNAs), by post-transcriptionally silencing EMT-related molecules, can promote or inhibit the EMT process and play pivotal roles in effectively manipulating the.

Prostate cancer PC3 cells undergo epithelial-mesenchymal

Frontiers | Increased Hemodynamic Load in Early Embryonic

Epithelial to mesenchymal transition as a paradigm of cell plasticity: Definition of EMT and introductory remarks. Epithelial-mesenchymal transitions under the lens. Molecular Mechanisms Involved in EMT. General concepts. E-cadherin downregulation: The major role of SNAI1 and GSK3 Indeed, they are able to promote epithelial-mesenchymal transition, a process of cellular reprogramming underlying tumor spread. In this manuscript, we review the currently known molecular mechanisms by which hepatitis viruses induce epithelial-mesenchymal transition and, thus, hepatocellular carcinoma progression Molecular mechanisms of 3,3′4,4′,5-pentachlorobiphenyl-induced epithelial-mesenchymal transition in human hepatocellular carcinoma cells Author links open overlay panel Li Song a Linlin Guo a Zhuoyu Li a Epithelial-mesenchymal transition (EMT) is a phenotypic conversion that facilitates organ morphogenesis and tissue remodeling. The authors of this Review discuss the phenomenon of EMT in. Mechanism of the Mesenchymal-Epithelial Transition and Its Relationship with Metastatic Tumor Formation Dianbo Yao, Chaoliu Dai, and Songlin Peng Abstract Cancer metastasis consists of a sequential series of events, and the epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) are recognized as critical events for metastasis of carcinomas. A current area of.

Epithelial-mesenchymal transition (EMT) encompasses dynamic changes in cellular organization from epithelial to mesenchymal phenotypes, which leads to functional changes in cell migration and. Epithelial-mesenchymal transition (EMT) is a reversible and dynamic process hypothesized to be co-opted by carcinoma during invasion and metastasis. Yet, there is still no quantitative measure to assess the interplay between EMT and cancer progression. Here, we derived a method for universal EMT scoring from cancer-specific transcriptomic EMT signatures of ovarian, breast, bladder, lung.

Molecular signature and therapeutic perspective of the epithelial-to-mesenchymal transitions in epithelial cancers. Sabbah M(1), Emami S, Redeuilh G, Julien S, Prévost G, Zimber A, Ouelaa R, Bracke M, De Wever O, Gespach C. Author information: (1)INSERM U673, Molecular and Clinical Oncology of Solid Tumors, Université Pierre et Marie Curie-Paris 6, Faculté de Médecine, Hôpital Saint. The transdifferentiation of epithelial cells into motile mesenchymal cells, a process known as epithelial-mesenchymal transition (EMT), is integral in development, wound healing and stem cell behaviour, and contributes pathologically to fibrosis and cancer progression. This switch in cell differentiation and behaviour is mediated by key transcription factors, including SNAIL, zinc-finger E.

The molecular mechanisms that drive EMT are complex and involve many more biochemical components. These have been reviewed extensively in . In addition to the biochemical signals, mechanical signals, such as the rigidity of the cell's microenvironment, also play roles in the regulation of EMT. Lee et al. observed that mammary epithelial cells underwent EMT when placed on hard substrates and. Molecular mechanism of miR‐153 inhibiting migration, invasion and epithelial‐mesenchymal transition of breast cancer by regulating transforming growth factor beta (TGF‐β) signaling pathway . Jingwei Wang. Department of Breast Surgery, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China. Search for more papers by this author. Shuhang Liang. Department of.

The morphological and molecular mechanisms of epithelial

  1. As one of the malignancies with high mortality and high insensitivity to existing therapies, pancreatic cancer and mechanisms underlying its progression have received growing scholarly attention. The role of the epithelial-mesenchymal transition (EMT) in pancreatic cancer genesis and metastasis has been reported albeit controversy has remained
  2. This volume details a comprehensive range of methods for imaging epithelial-to-mesechymal transition (EMT)/MET in in vivo systems, and methods to leverage these systems to dissect the underlying mechanisms.Chapters guide readers through studying different features of epithelial-mesenchymal plasticity, past and future research of the EMT, in vivo systems, and in vivo imaging
  3. Immunotherapy has offered a new opportunity for the treatment of many malignancies. In patients with lung cancer, immune checkpoint inhibitors have significantly improved survival. However, little is known about predictive factors or primary and acquired resistance mechanisms. Epithelial-to-mesenchymal transition (EMT) is a complex of phenotypic changes involved in carcinogenesis and.

The Molecular Mechanism of Epithelial-Mesenchymal

5.Martin, Molecular mechanisms of EMT regulation 6. different types of metastatic cancer cells 7. Methods for cTc and cTc cluster detection 8. Future perspectives 1. Introduction Epithelial-to-mesenchymal transition (EMT) is an evolution-arily conserved process that regulates the expression levels of various genes in epithelial cells that assume the mesenchymal phenotype. during the early. promotion of epithelial‐mesenchymal transition (EMT) when binding β‐catenin in GC. The role of Trop2 in promoting EMT in GC cells was examined by a variety of experimental assays. Moreover, the underlying molecular mechanism of Trop2 in promoting EMT was studied by in vivo and in vitro assays. The Trop2 expression i Epithelial-mesenchymal transition (EMT) is an important molecular mechanism contributing to fibrosis. Tubular epithelial cells (TEC), the major component of kidney parenchyma, are vulnerable to different types of injuries and as a significant source of myofibroblast by EMT. Furthermore, TRPC6 knockout plays an anti-fibrotic role in ameliorating kidney damage. However, the relationship between. Epithelial-mesenchymal transition (EMT) is an important process triggered during cancer metastasis. Regulation of EMT is mostly initiated by outside signalling, including TGF-β, growth factors, Notch ligand, Wnt, and hypoxia. Many signalling pathways have been delineated to explain the molecular mechanisms of EMT. In this review, we will focus on the epigenetic regulation of two critical EMT. Epithelial-to-Mesenchymal Transition may be classified into three 'types.' This classification takes into account the context in which the epithelial-to-mesenchymal transition occurs (Kalluri and Weinberg, 2009).Type 1 occurs during normal organogenesis, while type 2 occurs in the context of the healing process after injury: if the injury is mild and acute, the healing process is regarded.

[Molecular networks and mechanisms of epithelial

Epithelial-mesenchymal transition: molecular pathways of hepatitis viruses-induced hepatocellular carcinoma progression | springermedizin.de Skip to main conten The epithelial to mesenchymal transition (EMT) of malignant hepatocytes is a crucial event in hepatocellular carcinoma (HCC) progression and recurrence. We aimed to establish a human model of EMT to examine drug efficacy and specificity in HCC progression. Human HCC cell populations were characterized by immunofluorescence analysis, migration and invasion assays, array comparative genomic.

The process of epithelial-to-mesenchymal transition [EMT] The molecular mechanisms underlying chronic intestinal inflammation are complex and involve an intricate crosstalk between the immune system, epithelium and endothelium. 96 Understanding these mechanisms is of fundamental importance to design therapeutic strategies that are effective in limiting inflammation and the fibrogenic. Epithelial-mesenchymal transition in oral squamous cell carcinoma: An insight into molecular mechanisms and clinical implications. Address for correspondence: Dr. P Jayanthi, Department of Oral and Maxillofacial Pathology, Azeezia College of Dental Sciences and Research, Kollam, Kerala, India. E-mail: moc.liamg@pihtnayajrd An epithelial-mesenchymal transition (EMT) Moreover, it remains unclear at present whether these phenomena and molecular mechanisms relate to and explain the metastatic dissemination of non-epithelial cancer cells. Figure 5. Contribution of EMT to cancer progression. Progression from normal epithelium to invasive carcinoma goes through several stages. The invasive carcinoma stage involves. T1 - Molecular mechanisms regulating epithelial-to-mesenchymal transition and therapy sensitivity in breast cancer and glioblastoma. AU - Liang, Yuanke. PY - 2019. Y1 - 2019. N2 - This thesis is aimed at identifying novel therapeutic targets for breast cancer and aggressive brain tumors in preclinical models. Metastatic disease is the main cause of cancer-related deaths, including breast. epithelial-to-mesenchymal transition (EMT) and cancer stem cells (CSCs) play important roles during the develop-ment of drug resistance of prostate cancer. Unveiling the molecular mechanisms responsible for EMT and CSCs would help to develop new promising therapies for meta-static prostate cancer in the future. In this review, we wil

Mechanism of the Mesenchymal-Epithelial Transition and Its

Metastasis is frequently linked with reversible epithelial-to-mesenchymal transition (EMT), a process involved in tumor progression, and the formation of new distant metastatic sites (mesenchymal-to-epithelial transition or MET). On a single cell basis, cancer cells lose their epithelial features to gain mesenchymal characteristics via mechanisms influenced by the composition of the GSLs on. The small molecule SI113 hinders epithelial‐to‐mesenchymal transition and subverts cytoskeletal organization in human cancer cells . Claudia Abbruzzese. Division of Cellular Networks and Molecular Therapeutic Targets, Proteomics Unit, IRCCS—Regina Elena National Cancer Institute, Rome, Italy. Claudia Abbruzzese and Silvia Matteoni contributed equally to this work. Search for more papers. Molecular mechanisms of epithelial-mesenchymal transition Published in : Nature Reviews Molecular Cell Biology, February 2014 DOI: 10.1038/nrm3758: Pubmed ID: 24556840. Authors: Samy Lamouille, Jian Xu, Rik Derynck Abstract: The transdifferentiation of epithelial cells into motile mesenchymal cells, a process known as epithelial-mesenchymal transition (EMT), is integral in development, wound. Mechanism and regulation of epithelial-mesenchymal transition in cancer Irene K Guttilla ReedDepartment of Biology, University of Saint Joseph, West Hartford, CT, USAAbstract: During development and the pathogenesis of certain diseases, including cancer, the epithelial-mesenchymal transition (EMT) program is activated. It is hypothesized that EMT plays a major role in tumor invasion and.

Cells | Special Issue : Molecular and Cellular Mechanisms

Epithelial-to-mesenchymal transition (EMT) is a self-regulated physiological process required for tissue repair that, in non-controled conditions may lead to fibrosis, angiogenesis, loss of normal organ function or cancer. Although several molecular pathways involved in EMT regulation have been described, this process does not have any specific treatment Cellular and molecular mechanisms of renal fibrosis. Nature Reviews Nephrology, Vol. 7, Issue. 12, p. 684. CrossRef ; Google Scholar; Bolati, Dilinaer Shimizu, Hidehisa Higashiyama, Yukihiro Nishijima, Fuyuhiko and Niwa, Toshimitsu 2011. Indoxyl Sulfate Induces Epithelial-to-Mesenchymal Transition in Rat Kidneys and Human Proximal Tubular Cells. American Journal of Nephrology, Vol. 34, Issue. Epithelial-mesenchymal transition contributes to tumor progression by either generating migratory, invasive mesenchymal cancer cells or by the induction of stemness and generation of cancer stem cells, two processes that may involve similar phenomena, i.e., acquisition of stemness and mesenchymal characteristics. Possible epigenetic (classes of) drugs are illustrated to inhibit EMT, including. Epithelial-to-mesenchymal transition (EMT) is presently recognized as an important event and the initiating stage for tumor invasion and metastasis. Several EMT inducers have been identified, among which the big family of helix-loop-helix (HLH) transcription factors are rising as a novel and promising family of proteins in EMT mediation, such as Twist1, Twist2, E47, and HIFs, etc. Due to.

Epithelial-mesenchymal transition is a process in which epithelial cells downregulate epithelial and acquire mesenchymal features, as described for the first time by Elizabeth Hay (Fitchett and Hay 1989).By investigating the primitive streak of chicken embryos, she noticed that epithelial cells have the ability to transit to a mesenchymal state and can return to an epithelial state (Fitchett. Epithelial-mesenchymal transition (EMT) is a developmental process hijacked by cancer cells to modulate proliferation, migration, and stress response. Whereas kinase signaling is believed to be an EMT driver, the molecular mechanisms underlying epithelial-mesenchymal interconversion are incompletely understood. Here, we show that the impact of chromatin regulators on EMT interconversion is.

Molecular Analysis of Endothelial-mesenchymal Transition

Molecular mechanisms of endothelial to mesenchymal cell transition (EndoMT) in experimentally induced fibrotic diseases | springermedizin.de Skip to main conten Epithelial-mesenchymal transition (EMT) is a complex developmental program that enables carcinoma cells to suppress their epithelial features changing to mesenchymal ones. This change allows cells to acquire mobility and the capacity to migrate from the primary site. EMT provides a new insight for understanding the several steps of the metastatic process, from dedifferentiation to a more. Lung cancer (LC) is a leading cause of cancer-related death worldwide. Epithelial-mesenchymal transition (EMT) is a well-known phenomenon that promotes the invasive and metastatic capabilities of LC. Especially, EMT is assumed to be a pivotal mechanism for tumor cell invasion and metastasis, thereby limiting the efficacy of surgery and medical treatments, resulting in poor patient prognoses However, the molecular mechanism of CD133-regulated metastasis remains unclear. In recent years, epithelial-mesenchymal transition (EMT) has been linked to cancer invasion and metastasis. In the present study we investigated the role of CD133 in pancreatic cancer metastasis and its potential regulatory network. A highly migratory pancreatic cancer cell line, Capan1M9, was established.

Laboratories | Hokkaido University: Institute for Genetic

New insights into the mechanisms of epithelial-mesenchymal

  1. One possibility underlying the complexity of immunostain results in sarcomatoid UCa may be that tumors are undergoing epithelial-to-mesenchymal transition (EMT), a process that converts an epithelial phenotype to a motile, mesenchymal phenotype. 12,13 The EMT has been well described in a number of biologic paradigms, including embryogenesis, tissue fibrosis, and cancer, and is initiated.
  2. ation of tumor to distant metastatic sites. This review describes different signaling networks between.
  3. Molecular mechanisms of epithelial-mesenchymal transition. The transdifferentiation of epithelial cells into motile mesenchymal cells, a process known as epithelial-mesenchymal transition (EMT), is integral in development, wound healing and stem cell behaviour, and contributes pathologically to fibrosis and cancer progression

Nature reviews. Molecular cell biology, 2014-03, Vol.15 (3), p.178-196. Share Share Shar This article focuses on the molecular mechanisms through which TGF-β interacts with multiple intracellular signaling pathways in tumor progression and the effects of these interactions on tumorigenesis. The transforming growth factor-β (TGF-β) signaling pathway plays multiple regulatory roles in the tumorigenesis and development of cancer. TGF-β can inhibit the growth and proliferation of. Epithelial-mesenchymal transition (EMT) is one such multifaceted molecular program in malignant transformation which causes loss of epithelial characteristics and gain in mesenchymal phenotype. [3] EMT is believed to be a vital mechanism for carcinoma progression and is associated with aggressive behavior of cancer cells

Although numerous studies have examined the role of epithelial mesenchymal transition (EMT) in the pathogenesis of fibrotic disorders and there has been extensive investigation of the molecular events responsible for this process [28-31], studies examining the mechanisms involved in EndoMT and its potential participation in pathologic tissue fibrosis in human diseases are limited The Mechanism of a BMP-Driven Mesenchymal-to-Epithelial Transition during the Reprogramming of Induced Pluripotent Stem Cells Da Liu Master of Science Department of Molecular Genetics University of Toronto 2014 Abstract Somatic cells can be reprogrammed to induced pluripotent stem cells (iPSCs) by the ectopic expression of defined factors. iPSCs hold great promise for pharmaceutical screening.

Molecular mechanisms of 3,3′4,4′,5-pentachlorobiphenyl

Tumors showing evidence of epithelial-to-mesenchymal transition (EMT) have been associated with metastasis, drug resistance, and poor prognosis. Heterogeneity along the EMT spectrum is observed between and within tumors. To develop effective therapeutics, a mechanistic understanding of how EMT affects the molecular requirements for proliferation is needed Epithelial-mesenchymal transition, in which adherent epithelial cells differentiate into migratory mesenchymal cells, has been identified as an important step in the generation of tissues and organs. 1 Epithelial-mesenchymal transition has received much attention because it is involved in tumor progression, especially in several stages of the metastatic cascade including the loss of cell. This mechanism of intra-abdominal metastatic spread allows for the capture and molecular comparison of primary and metastatic cancer cells isolated from the same patient, providing a favorable opportunity to evaluate the potential role of epithelial-to-mesenchymal transition (EMT) in the metastatic process Basic molecular processes and signaling pathways contributing to the epithelial-mesenchymal transition (EMT). EMT is a developmental process by which epithelial cells lose their cell-cell adhesions and acquire mesenchymal cells identity. Loss of epithelial marker such as E-cadherin and the gain of mesenchymal marker such as Vimentin are considered as hallmarks in the initiation and execution. Introduction Epithelial to mesenchymal transition as a paradigm of cell plasticity: Definition of EMT and introductory remarks Epithelial-mesenchymal transitions under the lens Molecular Mechanisms..

Epithelial-mesenchymal transition (EMT) is a physiological process in which epithelial cells acquire the motile and invasive characteristics of mesenchymal cells. Although EMT in embryonic development is a coordinated, organized process involving interaction between many different cells and tissue types, aspects of the EMT program can be inappropriately activated in response to. Epithelial-mesenchymal transition (EMT) programs play essential functions in normal morphogenesis and organogenesis, including that occurring during mammary gland development and glandular regeneration. Historically, EMT programs were believed to reflect a loss of epithelial gene expression signatures and morphologies that give way to those associated with mesenchymal cells and their. It is known that epithelial-mesenchymal transition (EMT) is one of the key molecular steps in the process of distant metastasis. As the initial stage of metastatic progression, EMT is a complex process that includes not only dissolution of cell-cell junctions, but also loss of apicobasolateral polarity . During the EMT process, GC cells lose. Mechanisms of fibrogenesis in liver cirrhosis: The molecular aspects of epithelial-mesenchymal transition Sun-Jae Lee, Kyung-Hyun Kim, Kwan-Kyu Park Sun-Jae Lee, Kyung-Hyun Kim, Kwan-Kyu Park, Department of Pathology, Catholic University of Daegu, College of Medicine, Daegu, 705-718, South Korea Author contributions: Lee SJ and Park KK designed research; Lee SJ and Kim KH analyzed data; Lee SJ. Transforming growth factor-β1 (TGF-β1)‑induced epithelial‑mesenchymal transition (EMT) is one of the important cellular and molecular mechanisms involved in renal fibrosis. Smad3 and miR-192 (a Smad3-dependent microRNA) are involved in TGF-β1-mediated EMT. Vascular endothelial growth factor (VEGF) is a renal tubular epithelial survival factor

Epithelial-mesenchymal transition and drug resistance

  1. The epithelial-mesenchymal transition plays a critical role in cancer invasion and metastasis, and tumor metastasis is the major cause of lung cancer-related death. In a previous study, we reported that RNF8 played play an oncogenic role in breast cancer. In this study, using multiple lung cancer cell lines and validation with human lung.
  2. Distant disease involves multiple complex mechanisms, including invasion and migration, angiogenesis, anoikis resistance, and epithelial-mesenchymal transition (EMT) [3,4,5]. Therefore, a better understanding of such molecular mechanisms is required to facilitate the development of more accurate prognostic markers as well as effective therapeutic strategies [ 6 ]
  3. A mechanism by which GH may play this role in cancer is through the induction of the epithelial-to-mesenchymal transition (EMT). During the EMT process, epithelial cells lose their defining phenotypes, causing loss of cellular adhesion and increased cell migration. This review aims to carefully summarize the previous two decades of research that points to GH as an initiator of EMT, in both.
  4. g growth factor (TGF)-β plays a central role in the induction of EMT, the.
  5. e the roles of BMI-1 in inducing EMT of endometrial cancer (EC) cells and the possible role of.
  6. For most carcinomas, progression toward malignancy is accompanied by loss of epithelial differentiation and a shift towards a mesenchymal phenotype. This process, referred to as epithelial to mesenchymal transition (EMT), exacerbates motility and invasiveness of many cell types and is often considered a prerequisite for tumor infiltration and metastasis
  7. Although epithelial-to-mesenchymal transition (EMT) is a mechanism of resistance to various targeted drugs, its involvement in ALK inhibitor resistance is largely unknown. In this study, we report that both ALK-mutant L1196M and EMT were concomitantly detected in a single crizotinib-resistant lesion in a patient with ALK-rearranged lung cancer

Epithelial-mesenchymal transition - Wikipedi

Cancer cells undergo epithelial-mesenchymal transition (EMT) during invasion and metastasis. Although transforming growth factor-β (TGF-β) and pro-inflammatory cytokines have been implicated in EMT, the underlying molecular mechanisms remain to be elucidated. Here, we studied the effects of proinflammatory cytokines derived from the mouse macrophage cell line RAW 264.7 on TGF-β-induced EMT. Here, we re-visit epiboly in quail embryos and characterize several molecular markers of epithelial-to-mesenchymal transition (EMT) in the inner zone of the extraembryonic Area Opaca and at the blastoderm edge. Our results show that the intermediate filament vimentin, a widely-used marker for the mesenchymal phenotype, is strongly expressed in the edge cells compared to the cells in the inner. The epithelial-mesenchymal transition (EMT) comprises an essential biological process involving cancer progression as well as initiation. While the EMT has been regarded as a phenotypic conversion from epithelial to mesenchymal cells, recent evidence indicates that it plays a critical role in stemness, metabolic reprogramming, immune evasion and therapeutic resistance of cancer cells Partial epithelial mesenchymal transition (p-EMT) was found to play a potential role in the initial stage of metastasis in human head and neck squamous cell carcinoma (HNSCC). Some long noncoding RNAs (lncRNAs) have been reported to function as promoters or inhibitors of cancer metastasis. This study aimed to identify p-EMT-related lncRNAs in HNSCC

Leaving the neighborhood: molecular mechanisms involved

Here, we reveal that Menin overexpression leads to epithelial-mesenchymal transition (EMT) and the downregulation of CCAAT/enhancer binding protein (C/EBP) beta (C/EBPβ) in a histone-deacetylation manner. We also demonstrate that Menin acts as an EMT promoter or growth suppressor and interferes TGF-β signaling for EMT process, depending on the absence or presence of C/EBPβ. These data. Lamouille S, Xu J, Derynck R. Molecular mechanisms of epithelial-mesenchymal transition. Nature reviews Molecular cell biology. 2014;15(3):178. pmid:24556840 . View Article PubMed/NCBI Google Scholar 48. West AC, Johnstone RW. New and emerging HDAC inhibitors for cancer treatment. The Journal of clinical investigation. 2014;124(1):30. pmid.

IJMS | Free Full-Text | Emerging Therapeutics to OvercomeRecent advances in understanding liver fibrosisCellular and molecular mechanisms of tooth rootVaccines | Free Full-Text | Mesenchymal Stromal Cells Can
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