New insights into the mechanisms of epithelial mesenchymal transition and implications for cancer

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.. New insights into the mechanisms of epithelial-mesenchymal transition and implications for cancer. Nature Reviews Molecular Cell Biology ( IF 55.470 ) Pub Date : 2019-02-01 , DOI: 10.1038/s41580-018-0080-4. Anushka Dongre,Robert A Weinberg. Epithelial-mesenchymal transition (EMT) is a cellular programme that is known to be crucial for. These cells express molecules that are associated with the epithelial state and help maintain cell - New insights into the mechanisms of epithelial-mesenchymal transition and implications for cancer into the mechanism revealed EMT suppressed the expression of transporters and concentrating Box 1. What Is the Epithelial-to-Mesenchymal Transition? EMT is a transdifferentiation process in which epithelial cells lose their characteristics and instead take on properties (Figure 1, main text). EMT is a reversible process that depends on the synthetic effect In conclusion, recent evidence provides new insights into EMT in cancer, revealing that EMT is dispensable for cancer progression at least in the cancer models used and that EMT inhibition has synthetic effects with chemotherapy in metastasis suppression 6, 9. These results may redirect therapeutic explorations of EMT-targeting strategies and will stimulate future studies on the real roles of naturally occurring EMT in cancer initiation and progression

Epithelial-mesenchymal transition (EMT) is a form of cell plasticity in which epithelia acquire mesenchymal phenotypes and is increasingly recognized as an integral aspect of tissue fibrogenesis. In this review, we describe recent insight into the molecular and cellular factors that regulate EMT and its underlying signaling pathways. We also consider how mechanical cues from the microenvironment affect the regulation of EMT. Finally, we discuss the role of EMT in fibrotic. increased interest in the mechanisms by which cancer cells undergoing epithelial-mesenchymal transition (EMT), or oscillating within the EMT spectrum, might contribute to immune escape through multiple routes. This includes shaping of the TME and decreased susceptibility to immune effec-tor cells. Although much remains to be learned on the mechanisms at play An infection also leads to the progression of epithelial-mesenchymal transition within gastric tissue, increasing the probability of gastric cancer development. This paper aims to review the role of H. pylori and its virulence factors in epithelial-mesenchymal transition associated with malignant transformation within the gastric stroma Clinical Importance of EMT and MET. EMT is believed to be a major mechanism by which cancer cells become migratory and invasive, enabling the dissemination of cancer cells ( 4 ). In the EMT process, epithelial cells acquire fibroblast-like properties and show reduced intercellular adhesion and increased motility ( 4 ) The role of the epithelial-mesenchymal transition (EMT) in pancreatic cancer genesis and metastasis has been reported albeit controversy has remained. Recent insights into further EMT-regulating mechanisms underlying pancreatic cancer contribute to the nexus between EMT and this cancer type

Epithelial-mesenchymal transition in oral squamous cell carcinoma: An insight into molecular mechanisms and clinical implications. Epithelial-mesenchymal transition (EMT) is an important event in embryonic development, fibrosis and cancer invasion. During cancer progression, the activation of EMT permits cancer cells to acquire migratory, invasive. Molecular mechanisms of therapeutic resistance in CRC continue to be under intense investigation. In this review, we highlight the recent evidence linking epithelial-to-mesenchymal transition (EMT) with aggressive tumor biology as well as with the cancer stem cells (CSCs) across multiple organ systems including colon cancer

The epithelial-mesenchymal transition (EMT) is closely associated with the acquisition of aggressive traits by carcinoma cells and is considered responsible for metastasis, relapse, and chemoresistance. Molecular links between the EMT and cancer stem cells (CSCs) have indicated that EMT processes play important roles in expression of CSC-like properties. It is generally thought that EMT-related transcription factors (EMT-TFs) need to be downregulated to confer an epithelial. New Insights into the Implication of Epigenetic Alterations in the EMT of Triple Negative Breast Cancer. Cancers, MDPI, 2019, 11 (4), pp.559. ￿10.3390/cancers11040559￿. ￿hal-02349588￿ cancers Review New Insights into the Implication of Epigenetic Alterations in the EMT of Triple Negative Breast Cancer Noura Khaled * and Yannick Bidet Laboratoire d'Oncologie Moléculaire, Centre Jean. Epithelial-mesenchymal interaction refers to proximate paracrine cross-talk between tissue epithelia and stromal fibroblasts and is completely different from the concept of epithelial-mesenchymal transition (EMT). EMT is a variant of transdifferentiation and a well-recognized mechanism for dispersing cells in vertebrate embryos ( 17 ), forming.

The epithelial-mesenchymal transition (EMT) is closely associated with the acquisition of aggressive traits by carcinoma cells and is considered responsible for metastasis, relapse, and chemoresistance. Molecular links between the EMT and cancer stem cells (CSCs) have indicated that EMT processes play important roles in the expression of CSC-like properties. It is generally thought that EMT-related transcription factors (EMT-TFs) need to be downregulated to confer an epithelial. Epithelial-mesenchymal transition provides a new basis for understanding the progression of carcinoma towards dedifferentiated and more malignant states. You have full access to this article via.

New Insights into the Epithelial-to-Mesenchymal Transition

  1. New insights into the mechanisms of epithelial-mesenchymal transition and implications for cancer. Nat. Rev. Mol. Cell Biol. 2019; 20 : 69-84 View in Articl
  2. Ovarian cancer is known as a serious malignancy that affects women's reproductive tract and can considerably threat their health. A wide range of molecular mechanisms and genetic modifications have been involved in ovarian cancer pathogenesis making it difficult to develop effective therapeutic platforms. Hence, discovery and developing new therapeutic approaches are required. Medicinal plants, as a new source of drugs, could potentially be used alone or in combination with.
  3. Recent insights into the role of cancer stem cells (CSCs) and the epithelial-mesenchymal transition (EMT) in tumorigenesis have increased the knowledge base and highlighted new therapeutic targets of this disease. The process of EMT is regulated by a complex network of cytokines, transcription factors, growth factors, signaling pathways, and the tumor microenvironment, exhibiting CSC-like.
  4. The mechanical properties of epithelial to mesenchymal transition (EMT) and a pancreatic cancer subpopulation with stem cell properties have been increasingly recognized as potent modulators of the effective of therapy. In particular, pancreatic cancer stem cells (PCSCs) are functionally important during tumor relapse and therapy resistance

New Insights into the Regulation of Epithelial-Mesenchymal

  1. Circular RNAs in cancer: new insights into functions and implications in ovarian cancer . Zahra Shabaninejad 1,2 na1, Asma Vafadar 3 na1, Ahmad Movahedpour 3,4, Younes Ghasemi 2,3,5, Afshin Namdar 6, Hadis Fathizadeh 7, Mohammad Hossein Pourhanifeh 8, Amir Savardashtaki 2,3 & Hamed Mirzaei 8 Journal of Ovarian Research volume 12, Article number: 84 (2019) Cite this article. 1803 Accesses. 60.
  2. Epithelial-mesenchymal transition (EMT) is involved in physiologic processes such as embryogenesis and wound healing. A similar mechanism occurs in some tumors where cells leave the epithelial layer and gain mesenchymal particularities in order to easily migrate to other tissues. This process can explain the invasiveness and aggressiveness of these tumors which metastasize, by losing the.
  3. Epithelial-mesenchymal transitions under the lens. Molecular Mechanisms Involved in EMT. General concepts. E-cadherin downregulation: The major role of SNAI1 and GSK3β. Major signaling mechanisms related to growth factors acting on tyrosine kinase receptors. TGF β, Wnt/β-catenin, and ECM-related signaling in EM
  4. The epithelial-mesenchymal transition (EMT) is an orchestrated series of events in which cell-cell and cell-extracellular matrix (ECM) interactions are altered to release epithelial cells from the surrounding tissue, the cytoskeleton is reorganized to confer the ability to move through a three-dimensional ECM, and a new transcriptional program is induced to maintain the mesenchymal phenotype
  5. An epithelial-mesenchymal transition (EMT) is a biologic process that allows a polarized epithelial cell, which normally interacts with basement membrane via its basal surface, to undergo multiple biochemical changes that enable it to assume a mesenchymal cell phenotype, which includes enhanced migratory capacity, invasiveness, elevated resistance to apoptosis, and greatly increased production.
  6. Epithelial-mesenchymal transition (EMT) is an essential mechanism of metastasis, including in colorectal cancer. Although EMT processes are often triggered in cancer cells by their surrounding microenvironment, how EMT-relevant genes control these processes is not well understood. In multiple types of cancers, the transcription factor MEF2D has been implicated in cell proliferation, but its.

New insights into the role of EMT in tumor immune escap

Role of epithelial-mesenchymal transition EMT is an evolutionary-conserved process that can be activated in cancer cells and is linked to their dissociation from the primary tumor mass and their intravasation into blood vessels [ 64 ] The epithelial-mesenchymal transition (EMT) is an essential mechanism in embryonic development and tissue repair. EMT also contributes to the progression of disease, including organ fibrosis and cancer. EMT, as well as a similar transition occurring in vascular endothelial cells called endothelial-mesenchymal transition (EndMT), results from the induction of transcription factors that alter. New insights into the role of EMT in tumor immune escape Stephane Terry1, increased interest in the mechanisms by which cancer cells undergoing epithelial-mesenchymal transition (EMT), or oscillating within the EMT spectrum, might contribute to immune escape through multiple routes. This includes shaping of the TME and decreased susceptibility to immune effec-tor cells. Although much. New insights into the mechanisms of epithelial-mesenchymal transition and implications for cancer. Nat Rev Mol Cell Biol 2019 ; 20 : 69 - 84 . OpenUrl PubMe

Mechanisms of the Epithelial-Mesenchymal Transition and

This epithelial-mesenchymal plasticity (EMP) is underpinned by the processes of epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET). Both EMTs and METs are crucial for the migration and organization of many cell types into tissues and organs during embryogenesis New insights into the mechanisms of epithelial-mesenchymal transition and implications for cancer. Nat Rev Mol Cell Biol. 2019;20(2):69-84. CAS Article Google Scholar 13. Colak S, Ten Dijke P. Targeting TGF-β signaling in Cancer. Trends Cancer. 2017;3(1):56-71. CAS Article Google Scholar 14. Thiery JP, Acloque H, Huang RYJ, Nieto MA. Epithelial-mesenchymal transitions in development and. Here, we investigate coupled dynamics of epithelial-mesenchymal transition (EMT) in breast cancer cells and emergence of reversible drug resistance. Our mechanism-based model for the underlying regulatory network reveals that these two axes can drive one another, thus conferring bidirectional plasticity. This network can also enable non-genetic heterogeneity in a population of cells by. Colorectal cancer (CRC) is one of the most common cancers worldwide with a high incidence and mortality rate. Integrative studies including systematic sequencing of colorectal tumors have provided an unprecedented insight into the molecular basis of CRC. Recently, evidence indicates that F-box proteins (FBPs) play a critical role in the oncogenesis, invasion, metastasis and prognostic.

Reversible Epithelial to Mesenchymal Transition and

Mechanism of the Mesenchymal-Epithelial Transition and Its

Breast cancer relapse, in a large number of patients, after initial response to standard of care therapy warrants development of novel therapies against recurrent and metastatic cancer. Cancer stem cells (CSCs), present in breast tumors while being intrinsically resistant to conventional therapy, have the ability to self renew and cause tumor recurrence Epithelial-mesenchymal transition was first recognized as a feature of embryogenesis by Betty Hay in the 1980s. EMT, and its reverse process, MET (mesenchymal-epithelial transition) are critical for development of many tissues and organs in the developing embryo, and numerous embryonic events such as gastrulation, neural crest formation, heart valve formation, secondary palate development. According to 2012 data, lung cancer was the first common cancer in the world with 1.825 million new cases and with a high mortality rate . Pathologically, lung cancer can generally be divided into non-small cell lung cancer (NSCLC), which accounts for 80% of the cases, and small cell lung cancer (SCLC), which is more malignant Triple-negative breast cancer (TNBC) remains the most challenging breast cancer subtype to treat. To date, therapies directed to specific molecular targets have rarely achieved clinically meaningful improvements in outcomes of patients with TNBC, and chemotherapy remains the standard of care. Here, we seek to review the most recent efforts to classify TNBC based on the comprehensive profiling. Increasing evidence indicates that epithelial-mesenchymal transition (EMT) can be regulated by microRNAs (miRNAs). miR-615-3p was shown to be involved in tumor development. However, the role of miR-615-3p in the metastasis of breast cancer remains largely unknown. The expression of miR-615-3p in breast cancer cells and tissues was assessed by qRT-PCR and situ hybridization assays

Frontiers Epithelial-Mesenchymal Transition and Its

Epithelial-mesenchymal transition in oral squamous cell

We overexpressed LAIR-1 in OS cell lines by lentiviral transfection and measured cell proliferation, epithelial-mesenchymal transition (EMT)-associated transcription factor expression, and cell migration. Furthermore, EMT-related energy metabolism was examined after LAIR-1 overexpression. We believe that our study provides novel insights into the role of LAIR-1 in OS To investigate the influence of fibroblast activation protein alpha (FAP) derived from cancer-associated fibroblasts (CAFs), as well as potential mechanism of epithelial mesenchymal transition (EMT), on gastric cancer (GC) progression. Correlation between CAFs-derived FAP and clinical results has been studied by using 60 GC cases. To confirm this relationship, SGC7901 cells were co-cultured. The metastatic process of ovarian cancer (OC) is almost exclusively defined by direct shedding of tumor cells into the abdominal cavity, followed by clustering into multicellular aggregates and posterior peritoneal anchorage. This process relies on dynamic intercellular interactions which are modified by epithelial- mesenchymal interconversions and, therefore, E-cadherin expression variability Long intergenic non-coding RNAs (lncRNAs) are a class of non-coding RNAs that are involved in gene expression regulation. Taurine up-regulated gene 1 (TUG1) is a cancer progression related lncRNA in some tumor oncogenesis; however, its role in colorectal cancer (CRC) remains unclear. In this study, we determined the expression patterns of TUG1 in CRC patients and explored its effect on CRC.

Epithelial-to-mesenchymal transition and the cancer stem

Fatty acid synthase (FASN) is highly expressed in various types of cancer and has an important role in carcinogenesis and metastasis. To clarify the mechanisms of FASN in liver cancer invasion and metastasis, the FASN protein interaction network in liver cancer was identified by targeted proteomic analysis. Wound healing and Transwell assays was performed to observe the effect of FASN during. Ground-breaking discoveries in Tumor Biology uncovered novel mechanisms of epithelial-mesenchymal transition, transcriptional control of cancer drug sensitivity, epigenetic regulation of inflammation, novel mechanisms of androgen-resistance in prostate cancer, and immune evasion by viral mimicry. New targets were translated to the clinic in collaboration with other Programs for early detection. Dr. Palena's research focuses on the immunological targeting of drivers of tumor metastasis and resistance to therapy. Her recent studies on a novel tumor-associated antigen, the transcription factor brachyury, have led to the rapid translation of 3 cancer vaccine platforms targeting a driver of the epithelial-mesenchymal transition, a process associated with cancer Developmental Insights into Lung Cancer. Home Annual Review of Cancer Biology Volume 5, 2021 the mechanisms of lung cancer initiation, evolution, spread, and resistance are being unraveled at unprecedented resolution. Increasingly sophisticated mouse genetic, xenotransplantation, and ex vivo assays are also enabling functional validation and empiric screening of new therapeutic candidates. Purpose: Besides its therapeutic effects, chemotherapeutic agents also enhance the malignancy of treated cancers in clinical situations. Recently, epithelial-mesenchymal transition (EMT) has attracted attention in studies of tumor progression. We aimed to test whether transient Adriamycin treatment induces EMT and apoptosis simultaneously in cancer cells, clarify why the same type of cells.

Frontiers Communication Between Epithelial-Mesenchymal

New Insights into the Implication of Epigenetic

To understand this mechanism, Özlü and her team took human breast epithelial cells and by using one of the transition factors that play a role in epithelial-mesenchymal transition and control. Figure 2 Mechanism of epithelial-to-mesenchymal transition in colorectal cancer. External stimuli or mutations in cancer cells induce epithelial-to-mesenchymal transition (EMT), where epithelial cells undergo phenotypic changes and transit into an invasive mesenchymal cell state

Epithelial-mesenchymal transition and its implications for

Communication Between Epithelial-Mesenchymal Plasticity

Precision medicine has shed new light on the treatment of heterogeneous cancer patients. However, intratumor heterogeneity strongly constrains the clinical benefit of precision medicine. Thus, rethinking therapeutic strategies from a different facet within the precision medicine framework will not only diversify clinical interventions, but also provide an avenue for precision medicine Methods Two soluble factors that mediate tumor cell plasticity in the context of epithelial-mesenchymal transition are interleukin 8 (IL-8) and transforming growth factor beta (TGF-β). In an attempt to overcome escape mechanisms mediated by these cytokines, here we investigated the use of a small molecule inhibitor of the IL-8 receptors CXCR1/2, and a bifunctional agent that simultaneously. Pinpointing how cancer cells turn aggressive: Scientists have developed a new method for tracing the lineage and gene expression patterns of metastatic cancer at the single-cell level.

Epithelial-mesenchymal transitions in tumour progression

ITGB1 enhances the Radioresistance of human Non-small Cell Lung Cancer Cells by modulating the DNA damage response and YAP1-induced Epithelial-mesenchymal Transition . Yuexian Li 1, Cheng Sun 1, Yonggang Tan 1, Heying Zhang 1, Yuchao Li 2, Huawei Zou 1 . 1. Department of Oncology, Shengjing Hospital affiliated with China Medical University. The transition of prostate cancer away from a luminal epithelial phenotype is facilitated by genomic loss of the tumor suppressors RB1 and TP53, leading to changes in stem cell, developmental, and EMT programs, mediated in part by the lineage pluripotency transcription factor SOX2 ().Downregulation of REST (a transcription factor that normally silences the expression of neuron-specific genes.

Emerging Mechanisms by which EMT Programs Control Stemness

Epithelial-mesenchymal transition (EMT) is a critical biological process allowing epithelial cells to de-differentiate into mesenchymal cells. Orchestrated signaling pathways cooperatively induce EMT and effect physiological, sometimes pathological outcomes. Traditional Chinese Medicine (TCM) has been clinically prescribed for thousands of years and recent studies have found that TCM. Results of these studies will provide major new insights into the differential functional and biological roles of AT1 and AT2 cells in normal adult alveolar epithelium and during injury/recovery. Understanding how AT1 and AT2 cells in the adult lung maintain and differentiate their cellular functions, fates and lineages will constitute major advances in alveolar cell biology and could.

Sohal S, Reid D, Soltani A, et al. Evaluation of epithelial mesenchymal transition in patients with chronic obstructive pulmonary disease. Respir Res. 2011;12:130. 70. Wang H, Zhang H, Tang L, et al. Resveratrol inhibits TGF-1-induced epithelial-to-mesenchymal transition and suppresses lung cancer invasion and metastasis. Toxicology. 2013;303. The epithelial-mesenchymal transition (EMT) is associated with the suppression of sirtuin 3 (Sirt3) and aberrant glycolysis. Here, we hypothesized that the SGLT2 inhibitor empagliflozin restores normal kidney histology and function in association with the inhibition of aberrant glycolysis in diabetic kidneys. CD-1 mice with streptozotocin-induced diabetes displayed kidney fibrosis that was. Significant evidence has shown that the miRNA pathway is an important component in the downstream signaling cascades of TGF-β1 pathway. Our previous study has indicated that miR-335-5p expression was significantly down-regulated and acted as a vital player in the metastasis of non-small cell lung cancer (NSCLC), however the underlying mechanism remained unclear

Quercetin and cancer: new insights into its therapeutic

Our previous study had proved that nigericin could reduce colorectal cancer cell proliferation in dose- and time-dependent manners by targeting Wnt/β-catenin signaling. To better elucidate its potential anti-cancer mechanism, two pancreatic cancer (PC) cell lines were exposed to increasing concentrations of nigericin for different time periods, and the high-throughput sequencing was performed. recent research provided new insights into their impor-tance in cancer, (b) glucose transporter targeting, (c) the role of glucose transporters in the tumor microen-vironment, and (d) possible functions for glucose carri-ers beyond glucose uptake for glycolysis. Mechanisms of GLUT1 and GLUT3 regulation Tumor cells are known to have accelerated metabolic rates and high glucose demand in a. Prostate cancer (PCa) is the second leading cause of mortality and a leading cause of malignant tumors in males. Prostate cancer stem cells (PCSCs) are likely the responsible cell types for cancer initiation, clinical treatment failure, tumor relapse, and metastasis. Estrogen receptor alpha (ERα) is mainly expressed in the basal layer cells of the normal prostate gland and has key roles in.

Colorectal cancer (CRC) is the third most common cancer in men and the second in women worldwide [].Even after a continuous decline in the past 10 years, the estimated number of new cancer cases and deaths of CRC in the United States are 142,820 (9%) and 50,830 (9%) in 2013 [].Although great progress have been made in the diagnosis and treatment, surgery remains the only curative option and. The cancer stem cell (CSC) hypothesis postulates that cancer originates from the malignant transformation of stem/progenitor cells and is considered to apply to many cancers, including liver cancer. Identification that CSCs are responsible for drug resistance, metastasis, and secondary tumor appearance suggests that these populations are novel obligatory targets for the treatment of cancer A crucial event occurring in the metastatic process is the epithelial-mesenchymal transition (EMT), which endows tumor cells with the ability to trans-differentiate from epithelial to mesenchymal-like cells and to acquire the capability to leave the primary tumor mass and disseminate at distant sites (1, 2). EMT has been extensively linked to both metastatic progression of cancer (1, 3) and. Insights into cancer metastasis from a clinicopathologic perspective: Epithelial-mesenchymal transition is not a necessary step. Int J Cancer 132 : 1487 - 1495 . CrossRef Medline Google Schola Cancer stem cells (CSCs) play a critical role in tumor development and progression and are involved in cancer metastasis. The role of reactive oxygen species (ROS) in CSCs and cancer metastasis remains controversial. The aim of the present study was to investigate the correlation between ROS level of CSCs and cancer metastasis and to explore the possible underlying molecular mechanisms Cancer metastasis is a multi-step process that includes local invasion, intravasation to the lymph and blood systems, survival in the bloodstream, extravasation from the microvessels and colonization at a secondary site , . Numerous studies have revealed the insight into the mechanisms of each step of cancer metastasis ,

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