Wf-536 prevents tumor metastasis by inhibiting both tumor motility and angiogenic actions.

  title={Wf-536 prevents tumor metastasis by inhibiting both tumor motility and angiogenic actions.},
  author={Masahide Nakajima and Kazutaka Hayashi and Ken-ichi Katayama and Yusaku Amano and Yasuhiro Egi and Masayoshi Uehata and Nobuharu Goto and Takao Kondo},
  journal={European journal of pharmacology},
  volume={459 2-3},

The Rho kinase inhibitor fasudil inhibits tumor progression in human and rat tumor models

Fasudil, an orally available inhibitor of Rho kinases, and its metabolite 1-(hydroxy-5-isoquinoline sulfonyl-homopiperazine) (fasUDil-OH) modify tumor cell morphology and inhibit tumor cell migration and anchorage-independent growth.

The Rho kinase inhibitor fasudil inhibits the migratory behaviour of 95-D lung carcinoma cells.

Loss of RhoA expression prevents proliferation and metastasis of SPCA1 lung cancer cells in vitro.

RhoA inhibits apoptosis and increases proliferation of cultured SPCA1 lung cancer cells

It is suggested that RhoA knockdown prevents cell proliferation and induces apoptosis in SPCA1 lung cancer cells, and the underlying mechanisms responsible for these effects may include the activation of caspase-3 and the reduction of phospho-STAT3 levels.

The Rho-kinase inhibitor inhibits proliferation and metastasis of small cell lung cancer.

Effect of fasudil on growth, adhesion, invasion, and migration of 95D lung carcinoma cells in vitro.

The Rho-kinase inhibitor prevents the growth, adhesion, invasion, and migration of 95D lung carcinoma cells by inhibiting the Rho/Rho-Kinase pathway.

Rho Kinase Inhibitor Fasudil Suppresses the Vasculogenic Mimicry of B16 Mouse Melanoma Cells Both In Vitro and In Vivo

Investigating the biologic role of the Rho kinase inhibitor fasudil in the vasculogenic mimicry (VM) of B16 mouse melanoma cells and exploring the effect of RhoA and Rho-associated, coiled-coil containing protein kinase (ROCK) on VM formation suggest that fasUDil may be an emerging therapeutic option for targeting cancer VM.

Rho/ROCK signaling in motility and metastasis of gastric cancer.

This review discusses Rho GTPases and ROCK signaling and describes the mechanisms of Rho/ROCK activity with regard to motility and metastasis in gastric cancer and provides an insight of the therapeutic potential of targeting the Rho-associated protein kinases pathway.

6-Substituted purines as ROCK inhibitors with anti-metastatic activity.




Rho-kinase inhibitor retards migration and in vivo dissemination of human prostate cancer cells.

The Rho-kinase inhibitor, Y-27632, inhibited in vitro chemotactic migration to bone marrow fibroblast conditioned media and metastatic growth in immune-compromised mice of highly invasive human prostatic cancer (PC3) cells, and it is concluded that invasiveness of human prostate cancer is facilitated by the Rho/Rho-Kinase pathway.

Y‐27632, an Inhibitor of Rho‐associated Protein Kinase, Suppresses Tumor Cell Invasion via Regulation of Focal Adhesion and Focal Adhesion Kinase

Y‐27632 suppressed LPA‐induced tyrosine phosphorylation of FAK and paxillin, suggesting that ROCK regulates these molecules and Y‐276 32 inhibits cellular migration and morphological change, at least in part, through this regulation.

Inhibition of gelatinase A (MMP‐2) by batimastat and captopril reduces tumor growth and lung metastases in mice bearing Lewis lung carcinoma

The hypothesis of an essential role of metalloproteinase(s) in the metastatic process is supported and blockade of invasion, angiogenesis and other processes mediated by metalliproteinases may underlie the anti‐tumor and anti‐metastatic effect of BB‐94 and captopril and their combination.

Role of lysophosphatidic acid and rho in glioma cell motility.

The results suggest that LPA/Rho signaling cascades play important roles in glioma cell motility and that exposure of tumor cells to LPA in vivo may contribute to their invasive phenotype.

The suppression of small GTPase rho signal transduction pathway inhibits angiogenesis in vitro and in vivo.

Results suggest that inhibition of the small GTPase Rho signal transduction pathway by the p160ROCK inhibitor could be a possible new strategy for angiogenic diseases.

Molecular mechanisms of cancer metastasis: tumor and host properties and the role of oncogenes and suppressor genes

Together these tumor and host factors appear to determine the organ metastatic properties of malignant cells, which depend on multiple tumor cell, host cell, and stromal molecules that are differentially expressed by particular tumor and organ cells and by the organ extracellular matrix.

Distinct signal transduction pathways are utilized during the tube formation and survival phases of in vitro angiogenesis.

It is shown that HUVEC do not survive well in 3-D collagen gels due to rapid induction of apoptosis and VEGF, a potent in vivo angiogenic factor, fails to induce tube formation.

Tyrosine phosphorylation of the vascular endothelial-growth-factor receptor-2 (VEGFR-2) is modulated by Rho proteins.

Results indicate that Rho proteins may play an important role in angiogenesis by modulating the tyrosine phosphorylation levels of VEGFR-2.