scholarly journals Control of Invasion by Epithelial-to-Mesenchymal Transition Programs during Metastasis

2019 ◽  
Vol 8 (5) ◽  
pp. 646 ◽  
Author(s):  
Gray W. Pearson
Keyword(s):  
Tumor Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Single Cells ◽  
Paracrine Signaling ◽  
Intrinsic Properties ◽  
Extrinsic Factors ◽  
Mesenchymal Transition ◽  
Cell State ◽  
Invasive Behavior ◽  
Collective Invasion

Epithelial-to-mesenchymal transition (EMT) programs contribute to the acquisition of invasive properties that are essential for metastasis. It is well established that EMT programs alter cell state and promote invasive behavior. This review discusses how rather than following one specific program, EMT states are diverse in their regulation and invasive properties. Analysis across a spectrum of models using a combination of approaches has revealed how unique features of distinct EMT programs dictate whether tumor cells invade as single cells or collectively as cohesive groups of cells. It has also been shown that the mode of collective invasion is determined by the nature of the EMT, with cells in a trailblazer-type EMT state being capable of initiating collective invasion, whereas cells that have undergone an opportunist-type EMT are dependent on extrinsic factors to invade. In addition to altering cell intrinsic properties, EMT programs can influence invasion through non-cell autonomous mechanisms. Analysis of tumor subpopulations has demonstrated how EMT-induced cells can drive the invasion of sibling epithelial populations through paracrine signaling and remodeling of the microenvironment. Importantly, the variation in invasive properties controlled by EMT programs influences the kinetics and location of metastasis.

PHENOTYPIC HETEROGENEITY IN DISSEMINATED PROSTATE CANCER TUMOR CELLS: IMPLICATIONS IN EPITHELIAL TO MESENCHYMAL TRANSITION

2009 ◽  
Vol 181 (4S) ◽  
pp. 756-756
Author(s):  
Theodore D Koreckij ◽  
Todd M Morgan ◽  
Paul H Lange ◽  
Ilsa Coleman ◽  
Roger Coleman ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Phenotypic Heterogeneity ◽  
Mesenchymal Transition ◽  
Cancer Tumor

scholarly journals EMT Regulation by Autophagy: A New Perspective in Glioblastoma Biology

Cancers ◽  
2019 ◽  
Vol 11 (3) ◽  
pp. 312 ◽  
Author(s):  
Barbara Colella ◽  
Fiorella Faienza ◽  
Sabrina Di Bartolomeo
Keyword(s):  
Transcription Factors ◽  
Tumor Cells ◽  
Tissue Repair ◽  
Epithelial To Mesenchymal Transition ◽  
Signalling Pathways ◽  
Migration And Invasion ◽  
Cell Resistance ◽  
Mesenchymal Phenotype ◽  
Mesenchymal Transition ◽  
New Perspective

Epithelial-to-mesenchymal transition (EMT) and its reverse process MET naturally occur during development and in tissue repair in vertebrates. EMT is also recognized as the crucial event by which cancer cells acquire an invasive phenotype through the activation of specific transcription factors and signalling pathways. Even though glial cells have a mesenchymal phenotype, an EMT-like process tends to exacerbate it during gliomagenesis and progression to more aggressive stages of the disease. Autophagy is an evolutionary conserved degradative process that cells use in order to maintain a proper homeostasis, and defects in autophagy have been associated to several pathologies including cancer. Besides modulating cell resistance or sensitivity to therapy, autophagy also affects the migration and invasion capabilities of tumor cells. Despite this evidence, few papers are present in literature about the involvement of autophagy in EMT-like processes in glioblastoma (GBM) so far. This review summarizes the current understanding of the interplay between autophagy and EMT in cancer, with special regard to GBM model. As the invasive behaviour is a hallmark of GBM aggressiveness, defining a new link between autophagy and EMT can open a novel scenario for targeting these processes in future therapeutical approaches.

Urothelial Carcinomas of the Urinary Bladder With Plasmacytoid or Rhabdoid Features and Tendency of Epithelial-Mesenchymal Transition in 3 Dogs

2018 ◽  
Vol 55 (5) ◽  
pp. 673-677 ◽  
Author(s):  
Susanne Je-Han Lin ◽  
Chi-Fei Kao ◽  
Fun-In Wang ◽  
Chian-Ren Jeng ◽  
Jih-Jong Lee ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Clinical Outcome ◽  
Tumor Cells ◽  
Epithelial Mesenchymal Transition ◽  
Limited Information ◽  
Mesenchymal Transition ◽  
Invasive Behavior ◽  
Urothelial Carcinomas ◽  
Rhabdoid Features ◽  
Malignant Behavior

Plasmacytoid and rhabdoid variants of urothelial carcinomas (UCs) of the urinary bladder have been described in humans with plasma cell–like or rhabdoid cellular appearance and aggressive clinical outcome. Canine UC of the bladder is generally classified as papillary/nonpapillary and infiltrating/noninfiltrating with limited information regarding other histological patterns. We report 3 cases of UC of the urinary bladder showing a unique discohesive cellular morphology with malignant behavior resembling the human plasmacytoid and rhabdoid variants of UC, which may raise some difficulties in diagnosis. Epithelial-mesenchymal transition and reduced E-cadherin expression were revealed by immunohistochemistry in 2 cases, possibly explaining the discohesive and invasive behavior of the tumor cells. The findings broaden the morphological spectrum as well as the distinct clinical features of canine UC of the urinary bladder.

scholarly journals Epithelial to Mesenchymal Transition: A Mechanism that Fuels Cancer Radio/Chemoresistance

Cells ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 428 ◽  
Author(s):  
József Dudás ◽  
Andrea Ladányi ◽  
Julia Ingruber ◽  
Teresa Bernadette Steinbichler ◽  
Herbert Riechelmann
Keyword(s):  
T Cells ◽  
Transcription Factors ◽  
Tumor Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Protein Translation ◽  
Therapy Resistance ◽  
Mesenchymal Transition ◽  
Rna Molecules ◽  
Tumor Microenvironments ◽  
Micro Rnas

Epithelial to mesenchymal transition (EMT) contributes to tumor progression, cancer cell invasion, and therapy resistance. EMT is regulated by transcription factors such as the protein products of the SNAI gene family, which inhibits the expression of epithelial genes. Several signaling pathways, such as TGF-beta1, IL-6, Akt, and Erk1/2, trigger EMT responses. Besides regulatory transcription factors, RNA molecules without protein translation, micro RNAs, and long non-coding RNAs also assist in the initialization of the EMT gene cluster. A challenging novel aspect of EMT research is the investigation of the interplay between tumor microenvironments and EMT. Several microenvironmental factors, including fibroblasts and myofibroblasts, as well as inflammatory, immune, and endothelial cells, induce EMT in tumor cells. EMT tumor cells change their adverse microenvironment into a tumor friendly neighborhood, loaded with stromal regulatory T cells, exhausted CD8+ T cells, and M2 (protumor) macrophages. Several EMT inhibitory mechanisms are instrumental in reversing EMT or targeting EMT cells. Currently, these mechanisms are also significant for clinical use.

scholarly journals Epithelial to Mesenchymal Transition (EMT) in a Laryngeal Squamous Cell Carcinoma of a Horse: Future Perspectives

Animals ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 2318
Author(s):  
Federico Armando ◽  
Francesco Godizzi ◽  
Elisabetta Razzuoli ◽  
Fabio Leonardi ◽  
Mario Angelone ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Tumor Cells ◽  
Squamous Cell ◽  
Epithelial To Mesenchymal Transition ◽  
Hpv Infection ◽  
Mesenchymal Transition ◽  
Human Squamous Cell Carcinoma ◽  
E6 Gene ◽  
Twist 1

Squamous cell carcinoma (SCC) is one of the most frequent tumors of skin and muco-cutaneous junctions in the horse. Equine papillomavirus type 2 (EcPV2) has been detected in equine SCC of the oral tract and genitals, and recently also in the larynx. As human squamous cell carcinoma of the larynx (SCCL), it is strongly etiologically associated with high-risk papillomavirus (h-HPV) infection. This study focuses on tumor cells behavior in a naturally occurring tumor that can undergo the so-called epithelial to mesenchymal transition (EMT). A SCCL in a horse was investigated by immunohistochemistry using antibodies against E-cadherin, pan-cytokeratin AE3/AE1, β-catenin, N-cadherin, vimentin, ZEB-1, TWIST, and HIF-1α. EcPV2 DNA detection and expression of oncogenes in SCC were investigated. A cadherin switch and an intermediate filaments rearrangement within primary site tumor cells together with the expression of the EMT-related transcription factors TWIST-1, ZEB-1, and HIF-1α were observed. DNA obtained from the tumor showed EcPV2 positivity, with E2 gene disruption and E6 gene dysregulation. The results suggest that equine SCCL might be a valuable model for studying EMT and the potential interactions between EcPV2 oncoproteins and the EMT process in SCCL.

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