4.5 Article

c-Met activation promotes extravasation of hepatocellular carcinoma cells into 3D-cultured hepatocyte cells in lab-on-a-chip device

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DOI: 10.1016/j.bbamcr.2023.119557

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HCC; c-Met; Metastasis; Extravasation; Lab-on-a-chip (LOC); Microenvironment

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This study investigated the role of aberrant c-Met activation in regulating the extravasation and homing capacity of hepatocellular carcinoma (HCC) cells using a Lab on a Chip device. It was found that c-Met overexpression and activation directed HCC cells towards the hepatocytes-enriched microenvironment, and blocking c-Met phosphorylation attenuated the extravasation and homing capacity of HCC cells.
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.

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