Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

RhoC is a member of the Rho GTPase family that is implicated in cancer progression by stimulating cancer cell invasiveness. Here we report that RhoC regulates the interaction of cancer cells with vascular endothelial cells (ECs), a crucial step in the metastatic process. RhoC depletion by RNAi reduces PC3 prostate cancer cell adhesion to ECs, intercalation between ECs as well as transendothelial migration in vitro. Depletion of the kinases ROCK1 and ROCK2, two known RhoC downstream effectors, similarly decreases cancer interaction with ECs. RhoC also regulates the extension of protrusions made by cancer cells on vascular ECs in vivo. Transient RhoC depletion is sufficient to reduce both early PC3 cell retention in the lungs and experimental metastasis formation in vivo. Our results indicate RhoC plays a central role in cancer cell interaction with vascular ECs, which is a critical event for cancer progression.

Original publication

DOI

10.1016/j.molonc.2015.01.004

Type

Journal article

Journal

Mol Oncol

Publication Date

06/2015

Volume

9

Pages

1043 - 1055

Keywords

Endothelial cells, ROCKs, Rho GTPases, RhoC, cancer metastasis, cell migration, Cell Communication, Cell Line, Tumor, Human Umbilical Vein Endothelial Cells, Humans, Neoplasms, rho GTP-Binding Proteins, rho-Associated Kinases, rhoC GTP-Binding Protein