New Insights into the Regulation of Epithelial–Mesenchymal Transition and Tissue Fibrosis

Lee, KangAe; Nelson, Celeste M.

doi:10.1016/b978-0-12-394305-7.00004-5

Cited by 154 publications

(181 citation statements)

References 295 publications

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“…Loss of E-cadherin is thought to be the prototypical marker of EMT 36 and is known to be regulated at both the transcriptional and post-transcriptional levels 37 . Several transcriptional factors, including Snail, Slug, Zeb-1 (ref.…”

Section: Elevated Pyk2 Expression Enhances Emt In Mammary Cellsmentioning

confidence: 99%

PYK2 sustains endosomal-derived receptor signalling and enhances epithelial-to-mesenchymal transition

et al. 2015

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Epithelial-to-mesenchymal transition (EMT) is a central developmental process implicated in cancer metastasis. Here we show that the tyrosine kinase PYK2 enhances cell migration and invasion and potentiates EMT in human breast carcinoma. EMT inducer, such as EGF, induces rapid phosphorylation of PYK2 and its translocation to early endosomes where it co-localizes with EGFR and sustains its downstream signals. Furthermore, PYK2 enhances EGF-induced STAT3-phosphorylation, while phospho-STAT3 directly binds to PYK2 promoter and regulates PYK2 transcription. STAT3 and PYK2 also enhance c-Met expression, while c-Met augments their phosphorylation, suggesting a positive feedback loop between PYK2-STAT3-c-Met. We propose that PYK2 sustains endosomal-derived receptor signalling and participates in a positive feedback that links cell surface receptor(s) to transcription factor(s) activation, thereby prolonging signalling duration and potentiating EMT. Given the role of EMT in breast cancer metastasis, we also found a significant correlation between PYK2 expression, tumour grade and lymph node metastasis, thus, demonstrating the clinicopathological implication of our findings.

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Section: Elevated Pyk2 Expression Enhances Emt In Mammary Cellsmentioning

confidence: 99%

PYK2 sustains endosomal-derived receptor signalling and enhances epithelial-to-mesenchymal transition

et al. 2015

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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%

“…It has a role in the organogenesis and wound healing, but also in disease pathogenesis such as fibrosis and cancer. The EMT hallmarks include loss of apicobasal orientation, decreased expression of adhesion molecules, matrix degradation and increased expression of mesenchymal markers (Lee and Nelson, 2012). There has been previously reported a connection between the EMT-inducing transcription factors twist, snail and zeb1 activation and the promotion of radioresistance in both non-small cell lung cancer (NSCLC) and breast cancer cells (Gomez-Casal et al, 2013;Zhang et al, 2014).…”

Section: Introductionmentioning

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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“…[2][3][4] We interpreted the differences observed in cells lines as an evidence reflecting their unique cell properties and our studies confirm widely accepted results. [5][6][7][8][9][10][11] The main point of criticism of author of the Comment is that "such measurements… may not accurately reflect physiological aspects of cell-cell adhesion." We would like to emphasize the fact that all in vitro studies involving cell culture are always limited in their physiological significance.…”

mentioning

confidence: 99%

Response to “Comment on ‘A method to measure cellular adhesion utilizing a polymer micro-cantilever’” [Appl. Phys. Lett. 104, 236103 (2014)]

Gaitas

Malhotra

Pienta

et al. 2014

Applied Physics Letters

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New Insights into the Regulation of Epithelial–Mesenchymal Transition and Tissue Fibrosis

Cited by 154 publications

References 295 publications

PYK2 sustains endosomal-derived receptor signalling and enhances epithelial-to-mesenchymal transition

PYK2 sustains endosomal-derived receptor signalling and enhances epithelial-to-mesenchymal transition

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

Response to “Comment on ‘A method to measure cellular adhesion utilizing a polymer micro-cantilever’” [Appl. Phys. Lett. 104, 236103 (2014)]

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