Epithelial–mesenchymal transition in lung development and disease: does it exist and is it important?

Bartis, Domokos; Miše, Nikica; Mahida, Rahul; Eickelberg, Oliver; Thickett, David

doi:10.1136/thoraxjnl-2013-204608

Cited by 273 publications

(219 citation statements)

References 88 publications

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“…Vimentin is specifically expressed in normal mesenchymal cells and overexpressed in lung cancer cells (26). In previous studies, vimentin has been considered as a marker for EMT (26), and EMT is considered to be involved in the pathogenesis of lung cancer (5). Insulin like growth factor 1 receptor-induced resistance to epidermal growth factor receptor-tyrosine kinase inhibitors in advanced NSCLC is mediated by EMT (27).…”

Section: Discussionmentioning

confidence: 99%

“…When EMT occurs, epithelial cells gradually transform into mesenchymal-like cells by losing their epithelial-associated functions and characteristics (5). Epigenetic downregulation of E-cadherin expression was observed in advanced NSCLC and restoration of E-cadherin expression strongly suppressed the invasion/migration of tumor cells (6,7).…”

Section: Introductionmentioning

confidence: 99%

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miR‑145‑5p inhibits epithelial‑mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non‑small cell lung cancer cells

et al. 2017

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Abstract. Lung cancer is one of the most common types of tumors and the leading cause of cancer-associated mortality in the world. Additionally, non-small cell lung cancer (NSCLC) accounts for ~80% of all lung cancer cases. Epithelialmesenchymal transition (EMT) is an important cell biological process, which is associated with cancer migration, metastasis, asthma and fibrosis in the lung. In the present study, it was revealed that miR-145-5p was able to suppress EMT by inactivating the c-Jun N-terminal kinase (JNK) signaling pathway in NSCLC cells. Mitogen-activated protein kinase kinase kinase 1 (MAP3K1) was predicted and confirmed to be a novel target of miR-145-5p. Overexpression of MAP3K1 was able to reverse the inhibition of EMT induced by miR-145-5p via the JNK signaling pathway. Overall, the results revealed that miR-145-5p inhibits EMT via the JNK signaling pathway by targeting MAP3K1 in NSCLC cells.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

miR‑145‑5p inhibits epithelial‑mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non‑small cell lung cancer cells

et al. 2017

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“…Previous data support the hypothesis that TGF-b1 induced by CSE activates Smad3 and ERK1/2, contributing to the EMT process in differentiated human bronchial epithelial cells. 27 We have recently shown that increased uPAR expression in the small airway epithelium of COPD patients participates in an active EMT process modulated by PI3K/ Akt and GSK3b. 17 uPAR is a glycosyl phosphatidylinositolanchored protein with a high affinity to uPA.…”

Section: Discussionmentioning

confidence: 99%

“…26 EMTrelated changes are described in other chronic epithelial stress, and are also present in the airway epithelia of COPD. 3,27 Several signaling factors have emerged as mediators of EMT that is associated with small airway fibrosis in COPD. Previous data support the hypothesis that TGF-b1 induced by CSE activates Smad3 and ERK1/2, contributing to the EMT process in differentiated human bronchial epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

Involvement of urokinase in cigarette smoke extract-induced epithelial–mesenchymal transition in human small airway epithelial cells

Wang

Zhang

et al. 2015

Laboratory Investigation

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Urokinase-type plasminogen activator (uPA) augments inflammation and tissue remodeling during lung injury and repair. The uPA expression in small airway epithelium of chronic obstructive pulmonary disease (COPD) increases. Epithelialmesenchymal transition (EMT) is important in the small airway fibrosis of COPD. This study shows the uPA regulation in cigarette smoke extract (CSE)-induced EMT in human small airway epithelial cell lines (HSAEpiCs). uPA is overexpressed in the small airway epithelium of COPD patients and CSE-treated cell lines. Furthermore, uPA expression correlated with vimentin expression in the small airway epithelium of COPD patients. uPA inhibition blocks CSE-induced EMT by reversing E-cadherin and a-catenin expression and retarding the induction of N-cadherin and vimentin, resulting in reduction in migration. uPA overexpression in HSAEpiC cells also promotes EMT and migration. EMT is partly reversed in uPA-overexpressing HSAEpiC cells through the silencing expression of uPA receptor. In conclusion, this study provides new insights into the contribution of uPA upregulation to EMT associated with small airway remodeling in COPD.

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“…During radon inhalation due to the low penetrating ability of the α-particles, only the uppermost layer of the epithelium is affected and potentially damaged. There are evidences supporting the involvement of EMT in the development of fibrosis and different types of cancer, including lung cancer (Bartis et al, 2014;Lee and Nelson, 2012;Zavadil and Böttinger, 2005). The EMT has been suggested to increase the invasiveness of already transformed tumour epithelial cells that have survived radiotherapy (Gomez-Casal et al, 2013;Xu et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Lack of epithelial-to-mesenchymal transition induction in two bronchial epithelial cell lines after alpha and gamma irradiation

Acheva

Eklund

Lemola

et al. 2015

IJLR

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Abstract:The induction of epithelial-to-mesenchymal transition (EMT) in human lung epithelial cell lines was investigated after α-particle and γ-radiation exposures. We applied TGF-β treatment of cells as positive EMT-controls and tested in parallel if radiation has a potentiating effect on the EMT induction. BEAS-2B and HBEC-3KT cells were irradiated with 5.4 MeV α-particles or γ-rays ( 60 Co, 1.13-1.15 Gy/min) with or without of TGF-β. The cells were harvested three days post treatment and the EMT markers vimentin, fibronectin and E-cadherin were analysed by immunofluorescence staining and Western blotting. The TGF-β treatment-induced EMT in both cell lines in the applied concentrations. We could not prove any clear EMT induction with low or moderate doses of α-particles and γ-rays. No significant additive effect with radiation and TGF-β was observed. We suggest that there might be a different mechanism induced by radiation in bronchial cells after radon and medical exposures that does not involve direct EMT changes.

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Epithelial–mesenchymal transition in lung development and disease: does it exist and is it important?

Cited by 273 publications

References 88 publications

miR‑145‑5p inhibits epithelial‑mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non‑small cell lung cancer cells

miR‑145‑5p inhibits epithelial‑mesenchymal transition via the JNK signaling pathway by targeting MAP3K1 in non‑small cell lung cancer cells

Involvement of urokinase in cigarette smoke extract-induced epithelial–mesenchymal transition in human small airway epithelial cells

Lack of epithelial-to-mesenchymal transition induction in two bronchial epithelial cell lines after alpha and gamma irradiation

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