c-Met activation promotes extravasation of hepatocellular carcinoma cells into 3D-cultured hepatocyte cells in lab-on-a-chip device
Creators
- 1. Izmir Biomed & Genome Ctr IBG, TR-35340 Balcova, Izmir, Turkiye
- 2. Izmir Inst Technol, Biotechnol & Bioengn Grad Program, TR-35430 Urla, Izmir, Turkiye
- 3. Izmir Tinaztepe Univ, Galen Res Ctr, TR-35400 Buca, Izmir, Turkiye
- 4. Izmir Inst Technol, Dept Mol Biol & Genet, TR-35430 Urla, Izmir, Turkiye
Description
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.
Files
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Files
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