c-Met activation promotes extravasation of hepatocellular carcinoma cells into 3D-cultured hepatocyte cells in lab-on-a-chip device
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c-Met activation promotes extravasation of hepatocellular carcinoma cells into 3D-cultured hepatocyte cells in lab-on-a-chip device. / Bagci, Gulsun; Comez, Dehan; Topel, Hande; Yilmaz, Yeliz; Bagirsakci, Ezgi; Gunes, Aysim; Batı Ayaz, Gizem; Tahmaz, Ismail; Bilgen, Muge; Solmaz, Gulhas; Pesen Okvur, Devrim; Atabey, Nese.
In: B B A - Molecular Cell Research, Vol. 1870, No. 8, 12.2023, p. 119557.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - c-Met activation promotes extravasation of hepatocellular carcinoma cells into 3D-cultured hepatocyte cells in lab-on-a-chip device
AU - Bagci, Gulsun
AU - Comez, Dehan
AU - Topel, Hande
AU - Yilmaz, Yeliz
AU - Bagirsakci, Ezgi
AU - Gunes, Aysim
AU - Batı Ayaz, Gizem
AU - Tahmaz, Ismail
AU - Bilgen, Muge
AU - Solmaz, Gulhas
AU - Pesen Okvur, Devrim
AU - Atabey, Nese
N1 - Copyright © 2023 Elsevier B.V. All rights reserved.
PY - 2023/12
Y1 - 2023/12
N2 - 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.
AB - 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.
KW - Humans
KW - Carcinoma, Hepatocellular/pathology
KW - Liver Neoplasms/genetics
KW - Hepatocytes
KW - Cell Line
KW - Tumor Microenvironment
U2 - 10.1016/j.bbamcr.2023.119557
DO - 10.1016/j.bbamcr.2023.119557
M3 - Journal article
C2 - 37549739
VL - 1870
SP - 119557
JO - B B A - Molecular Cell Research
JF - B B A - Molecular Cell Research
SN - 0167-4889
IS - 8
ER -
ID: 389913292