Loss of ezrin in human intrahepatic cholangiocarcinoma is associated with ectopic expression of E‐cadherin

Guedj, Nathalie; Vaquero, Javier; Clapéron, Audrey; Mergey, Martine; Chrétien, Yves; Paradis, Valérie; Fouassier, Laura

doi:10.1111/his.12931

Cited by 4 publications

(3 citation statements)

References 32 publications

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“…Therefore, these data indicated that Ezrin may also serve as a tumour suppressor. 29 The discordance between these studies suggested that the effects of Ezrin in different tumours may be different. Ezrin overexpression promotes BC progression via AKT signalling pathway.…”

Section: Discussionmentioning

confidence: 99%

Ezrin promotes breast cancer progression by modulating AKT signals

Kong

Lin

et al. 2019

Br J Cancer

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BACKGROUND: Ezrin, which is known as a cytoskeleton linker protein, is closely linked with the metastatic progression of cancer and is frequently abnormally expressed in aggressive cancer types. However, the possible involvement of Ezrin in metastasis and angiogenesis in breast cancer remains unclear. METHODS: Immunohistochemical analysis of Ezrin was performed on both BC samples (n = 117) and normal epithelium samples (n = 47). In vivo and in vitro assays were performed to validate the effect of Ezrin on AKT pathway-mediated BC progression. RESULTS: In this study, Ezrin was found to be upregulated in BC tissues, which was linked with aggressive tumour characteristics and poor prognosis. Moreover, we showed that Ezrin promotes BC proliferation, migration, invasion, and angiogenesis in vitro and in vivo. Mechanistic analysis showed that Ezrin interacted with AKT, and promoted its kinase activity, thereby regulating the AKT pathway in BC. CONCLUSIONS: In all, we propose a model for an Ezrin/AKT oncoprotein axis, which provides novel insight into how Ezrin contributes to BC progression.

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Section: Discussionmentioning

confidence: 99%

Ezrin promotes breast cancer progression by modulating AKT signals

Kong

Lin

et al. 2019

Br J Cancer

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“…Relocalisation of adherens junction component E-Cadherin from BEC membranes, implicates reduced cell adhesion and strongly supports this notion since mis-regulation of E-Cadherin levels is a hallmark of biliary diseases. BEC-specific deletion of E-Cadherin in mice causes cholangitis and cancer(Nakagawa et al ., 2014), while in biliary atresia and intrahepatic cholangiocarcinoma it is aberrantly expressed in BECs and hepatocytes (Guedj et al, 2016). The loss of E-cadherin at BEC membranes is also reminiscent of epithelial-to-mesenchymal transition, where E-cadherin reduction and upregulation of N-cadherin results in acquisition of mesenchymal migratory behaviours (Lamouille et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

LiverZap: A chemoptogenetic tool for global and locally restricted hepatocyte ablation to study cellular behaviours in liver regeneration

Ambrosio

Bailey

Unterweger

et al. 2023

Preprint

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The liver restores its mass and architecture after injury. Yet, investigating morphogenetic cell behaviours and signals that repair tissue architecture at high spatiotemporal resolution remains challenging. We developed LiverZap, a tuneable chemoptogenetic liver injury model in zebrafish. LiverZap employs formation of a binary FAP-TAP photosensitiser followed by brief near-infrared illumination inducing hepatocyte-specific death and recapitulating mammalian liver injury types. The tool enables local hepatocyte ablation and extended live imaging of regenerative cell behaviours, critical for studying cellular interactions at the interface of healthy and damaged tissue. Applying LiverZap, we show that targeted hepatocyte ablation in a small region-of-interest is unexpectedly sufficient to trigger Liver Progenitor-like Cell (LPC)-mediated regeneration, challenging the current understanding of LPC activation. Associated dynamic bilary network rearrangement and E-cadherin relocalisation suggest modulation of cell adhesion as an integral step of LPC-mediated liver regeneration. This precisely targetable live cell ablation model will enable addressing of key regeneration paradigms.

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“…A similar finding in breast cancer showed that high Ezrin and low E-cadherin expression were more related to lymph node metastasis and poor prognosis [ 93 ]. In contrast, in intrahepatic cholangiocarcinoma, lack of or low Ezrin expression is associated with ectopic expression of E-cadherin and may coincide with the activation of an EMT-like process [ 94 ].…”

Section: Ezrin Interacts With Metastasis-related Proteinsmentioning

confidence: 99%

Ez-Metastasizing: The Crucial Roles of Ezrin in Metastasis

Buenaventura,

Merlino,

2023

Cells

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Ezrin is the cytoskeletal organizer and functions in the modulation of membrane–cytoskeleton interaction, maintenance of cell shape and structure, and regulation of cell–cell adhesion and movement, as well as cell survival. Ezrin plays a critical role in regulating tumor metastasis through interaction with other binding proteins. Notably, Ezrin has been reported to interact with immune cells, allowing tumor cells to escape immune attack in metastasis. Here, we review the main functions of Ezrin, the mechanisms through which it acts, its role in tumor metastasis, and its potential as a therapeutic target.

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Loss of ezrin in human intrahepatic cholangiocarcinoma is associated with ectopic expression of E‐cadherin

Abstract: Ezrin is down-regulated during cholangiocarcinogenesis, and its loss results in a more aggressive phenotype.

Cited by 4 publications

References 32 publications

Ezrin promotes breast cancer progression by modulating AKT signals

Ezrin promotes breast cancer progression by modulating AKT signals

LiverZap: A chemoptogenetic tool for global and locally restricted hepatocyte ablation to study cellular behaviours in liver regeneration

Ez-Metastasizing: The Crucial Roles of Ezrin in Metastasis

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