Please use this identifier to cite or link to this item:
https://hdl.handle.net/11147/13830
Title: | c-Met activation promotes extravasation of hepatocellular carcinoma cells into 3D-cultured hepatocyte cells in lab-on-a-chip device | Authors: | Bağcı, Gülsün Çömez, Dehan Topel, Hande Yılmaz, Yeliz Bağırsakçı, Ezgi Güneş, Aysim Batı Ayaz, Gizem Tahmaz, İsmail Bilgen, Müge Solmaz, Gülhas Pesen Okvur, Devrim |
Keywords: | c-Met Extravasation HCC Lab-on-a-chip Metastasis Microenvironment |
Publisher: | Elsevier | Abstract: | Activation of c-Met signaling is associated with an aggressive phenotype and poor prognosis in hepatocellular carcinoma (HCC); however, its contribution to organ preference in metastasis remains unclear. In this study, using a Lab on a Chip device, we defined the role of aberrant c-Met activation in regulating the extravasation and homing capacity of HCC cells. Our studies showed that (i) c-Met overexpression and activation direct HCC cells preferentially towards the hepatocytes-enriched microenvironment, and (ii) blockage of c-Met phosphorylation by a small molecule inhibitor attenuated extravasation and homing capacity of HCC cells. These results, thus, demonstrate the role of c-Met signaling in regulating the colonization of HCC cells preferentially in the liver. © 2023 Elsevier B.V. | URI: | https://doi.org/10.1016/j.bbamcr.2023.119557 https://hdl.handle.net/11147/13830 |
ISSN: | 0167-4889 |
Appears in Collections: | Molecular Biology and Genetics / Moleküler Biyoloji ve Genetik PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection Scopus İndeksli Yayınlar Koleksiyonu / Scopus Indexed Publications Collection WoS İndeksli Yayınlar Koleksiyonu / WoS Indexed Publications Collection |
Files in This Item:
File | Size | Format | |
---|---|---|---|
1-s2.0-S0167488923001301-main.pdf | 1.97 MB | Adobe PDF | View/Open |
CORE Recommender
Page view(s)
172
checked on Nov 18, 2024
Download(s)
70
checked on Nov 18, 2024
Google ScholarTM
Check
Altmetric
Items in GCRIS Repository are protected by copyright, with all rights reserved, unless otherwise indicated.