C-Met Activation Promotes Extravasation of Hepatocellular Carcinoma Cells Into 3d-Cultured Hepatocyte Cells in Lab-On Device

Loading...

Date

Journal Title

Journal ISSN

Volume Title

Publisher

Open Access Color

Green Open Access

Yes

OpenAIRE Downloads

OpenAIRE Views

Publicly Funded

No
Impulse
Average
Influence
Average
Popularity
Average

relationships.isProjectOf

relationships.isJournalIssueOf

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.

Description

Keywords

c-Met, Extravasation, HCC, Lab-on-a-chip, Metastasis, Microenvironment, Microenvironment, Carcinoma, Hepatocellular, Lab-on-a-chip (LOC), Liver Neoplasms, Hepatocytes, Tumor Microenvironment, Humans, HCC, Extravasation, Metastasis, c-Met, Cell Line

Fields of Science

Citation

WoS Q

Scopus Q

OpenCitations Logo
OpenCitations Citation Count
2

Volume

1870

Issue

8

Start Page

End Page

PlumX Metrics
Citations

Scopus : 2

PubMed : 1

Captures

Mendeley Readers : 5

Google Scholar Logo
Google Scholar™
OpenAlex Logo
OpenAlex FWCI
0.59463301

Sustainable Development Goals