The Role of Epithelial-Mesenchymal Transition (EMT) in Cancer Development and Metastasis

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 2514

Special Issue Editor


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Guest Editor
Department of Biology, Texas A&M University, College Station, TX, USA
Interests: EMT; angiogenesis; vascular mimicry; tumor microenvironment; cancer bioinformatics

Special Issue Information

Dear Colleagues,

Benign tumor cells acquire infiltrating and metastasizing properties during tumor progression due to the epithelial to mesenchymal transition (EMT), which enhances tumors’ mobility, invasion, and resistance to apoptotic stimuli. EMT is known to generate cells with the properties of stem cells and according to a recent study carcinoma cells that have undergone an EMT differentiate into endothelial cells and contribute to tumor growth. Therefore, targeting EMT pathways constitutes an attractive strategy for cancer treatment. Major signaling pathways involved in EMT include transforming growth factor β(TGF-β), Wnt, Notch, Hedgehog, and other signaling pathways. These pathways are related to several transcription factors, including Twist, Smads and zinc finger proteins snail and slug. This Special Issue will focus on determining the functional role of EMT in metastasis, understanding the molecular mechanisms that regulate EMT-mediated tumor progression and metastasis, and the tools that are currently available for studying them both in vitro and in vivo (such as dynamic in vivo imaging, lineage tracing system, clinically relevant in vivo models, etc.).

Dr. Tapasree Roy Sarkar
Guest Editor

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Keywords

  • signaling networks guiding EMT
  • EMT and metastasis
  • in vivo models for studying EMT and metastasis
  • EMT and tumor vasculature
  • targeting EMT and cancer stem cells
  • EMT in metastasis and therapy resistance
  • cross-talk between EMT and autophagy
  • miRNA-mediated EMT
  • epigenetic regulation of EMT

Published Papers (1 paper)

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Research

16 pages, 1723 KiB  
Article
GLUT3 Promotes Epithelial–Mesenchymal Transition via TGF-β/JNK/ATF2 Signaling Pathway in Colorectal Cancer Cells
by Moon-Young Song, Da-Young Lee, Sun-Mi Yun and Eun-Hee Kim
Biomedicines 2022, 10(8), 1837; https://doi.org/10.3390/biomedicines10081837 - 29 Jul 2022
Cited by 12 | Viewed by 2230
Abstract
Glucose transporter (GLUT) 3, a member of the GLUTs family, is involved in cellular glucose utilization and the first step in glycolysis. GLUT3 is highly expressed in colorectal cancer (CRC) and it leads to poor prognosis to CRC patient outcome. However, the molecular [...] Read more.
Glucose transporter (GLUT) 3, a member of the GLUTs family, is involved in cellular glucose utilization and the first step in glycolysis. GLUT3 is highly expressed in colorectal cancer (CRC) and it leads to poor prognosis to CRC patient outcome. However, the molecular mechanisms of GLUT3 on the epithelial–mesenchymal transition (EMT) process in metastatic CRC is not yet clear. Here, we identified that activation of the c-Jun N-terminal kinase (JNK)/activating transcription factor-2 (ATF2) signaling pathway by transforming growth factor-β (TGF-β) promotes GLUT3-induced EMT in CRC cells. The regulation of GLUT3 expression was significantly associated with EMT-related markers such as E-cadherin, α- smooth muscle actin (α-SMA), plasminogen activator inhibitor-1 (PAI-1), vimentin and zinc finger E-box binding homeobox 1 (ZEB1). We also found that GLUT3 accelerated the invasive ability of CRC cells. Mechanistically, TGF-β induced the expression of GLUT3 through the phosphorylation of JNK/ATF2, one of the SMAD-independent pathways. TGF-β induced the expression of GLUT3 by increasing the phosphorylation of JNK, the nuclear translocation of the ATF2 transcription factor, and the binding of ATF2 to the promoter region of GLUT3, which increased EMT in CRC cells. Collectively, our results provide a new comprehensive mechanism that GLUT3 promotes EMT process through the TGF-β/JNK/ATF2 signaling pathway, which could be a potential target for the treatment of metastatic CRC. Full article
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