scholarly journals Epithelial-to-mesenchymal transition of murine liver tumor cells promotes invasion

Hepatology ◽  
2010 ◽  
Vol 52 (3) ◽  
pp. 945-953 ◽  
Author(s):  
Wei Ding ◽  
Hanning You ◽  
Hien Dang ◽  
Francis LeBlanc ◽  
Vivian Galicia ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Liver Tumor ◽  
Epithelial To Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Murine Liver

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.

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.

scholarly journals Consequences of EMT-Driven Changes in the Immune Microenvironment of Breast Cancer and Therapeutic Response of Cancer Cells

2019 ◽  
Vol 8 (5) ◽  
pp. 642 ◽  
Author(s):  
Snahlata Singh ◽  
Rumela Chakrabarti
Keyword(s):  
Breast Cancer ◽  
Tumor Progression ◽  
Tumor Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Therapeutic Response ◽  
Current Knowledge ◽  
Cell Contact ◽  
Invasive Potential ◽  
Mesenchymal Transition ◽  
Tumor Growth And Metastasis

Epithelial-to-mesenchymal transition (EMT) is a process through which epithelial cells lose their epithelial characteristics and cell–cell contact, thus increasing their invasive potential. In addition to its well-known roles in embryonic development, wound healing, and regeneration, EMT plays an important role in tumor progression and metastatic invasion. In breast cancer, EMT both increases the migratory capacity and invasive potential of tumor cells, and initiates protumorigenic alterations in the tumor microenvironment (TME). In particular, recent evidence has linked increased expression of EMT markers such as TWIST1 and MMPs in breast tumors with increased immune infiltration in the TME. These immune cells then provide cues that promote immune evasion by tumor cells, which is associated with enhanced tumor progression and metastasis. In the current review, we will summarize the current knowledge of the role of EMT in the biology of different subtypes of breast cancer. We will further explore the correlation between genetic switches leading to EMT and EMT-induced alterations within the TME that drive tumor growth and metastasis, as well as their possible effect on therapeutic response in breast cancer.

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