| First Author | Kim C | Year | 2014 |
| Journal | Cancer Cell | Volume | 25 |
| Issue | 1 | Pages | 102-17 |
| PubMed ID | 24434213 | Mgi Jnum | J:208154 |
| Mgi Id | MGI:5561176 | Doi | 10.1016/j.ccr.2013.12.010 |
| Citation | Kim C, et al. (2014) Vascular RhoJ is an effective and selective target for tumor angiogenesis and vascular disruption. Cancer Cell 25(1):102-17 |
| abstractText | Current antiangiogenic therapy is limited by its cytostatic nature and systemic side effects. To address these limitations, we have unveiled the role of RhoJ, an endothelial-enriched Rho GTPase, during tumor progression. RhoJ blockade provides a double assault on tumor vessels by both inhibiting tumor angiogenesis and disrupting the preformed tumor vessels through the activation of the RhoA-ROCK (Rho kinase) signaling pathway in tumor endothelial cells, consequently resulting in a functional failure of tumor vasculatures. Moreover, enhanced anticancer effects were observed when RhoJ blockade was employed in concert with a cytotoxic chemotherapeutic agent, angiogenesis-inhibiting agent, or vascular-disrupting agent. These results identify RhoJ blockade as a selective and effective therapeutic strategy for targeting tumor vasculature with minimal side effects. |
