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Updated: Apr 21, 2026
An Orthotopic Murine Model of Human Prostate Cancer Metastasis
Published on: September 18, 2013
Fasudil inhibits prostate cancer-induced angiogenesis in vitro
Weihua Chen1, Kaili Mao2, Thong Hua-Huy1
1Medical School, Service de Physiologie, Paris Descartes University, EA 2511, Hôpital Cochin, 75014 Paris, France.
Abstract:
Inhibition of angiogenesis is an important therapeutic strategy for advanced stage prostate cancer (PCa). RhoA/Rho-associated protein kinases (ROCK) are key regulators of the cytoskeleton and have been implicated in PCa angiogenesis. We investigated the anti-angiogenic effects of fasudil, a ROCK inhibitor, on PCa-induced angiogenesis in vitro. Proliferation of PCa-conditioned human umbilical vein endothelial cells (HUVECs) was assessed using a bromodeoxyuridine (BrdU) assay, and migration was assessed with a wound healing assay. In vitro angiogenesis of PCa-conditioned HUVECs was evaluated by tube formation and a spheroid sprouting assay. Fasudil inhibited PCa-induced endothelial cell proliferation at a concentration of 100 µM, and also decreased PCa-induced endothelial cell migration at a concentration of 30 µM. In the in vitro angiogenesis assay, fasudil exerted a more significant effect. Tube formation was significantly inhibited at fasudil concentrations exceeding 3 µM, and spheroid sprouts were significantly thinner and shorter (at fasudil concentrations of 10 and 30 µM, respectively). Western blotting results showed that expression of phosphorylated myosin phosphatase target subunit 1 (MYPT-1) was significantly lower after fasudil treatment, confirming that fasudil inhibited ROCK activity in these model systems. These data suggest that fasudil may be a useful anti-angiogenic agent for PCa.
Insights
Fasudil, a ROCK inhibitor, effectively reduced prostate cancer (PCa) cell proliferation, migration, and angiogenesis in vitro. This study highlights fasudil
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Angiogenesis inhibition is a key strategy for advanced prostate cancer (PCa).
- RhoA/Rho-associated protein kinases (ROCK) are implicated in PCa angiogenesis.
- ROCK signaling regulates the cytoskeleton, influencing cellular processes vital to tumor growth.
Purpose of the Study:
- To investigate the anti-angiogenic effects of fasudil, a ROCK inhibitor, on PCa-induced angiogenesis in vitro.
- To evaluate fasudil's impact on endothelial cell proliferation, migration, and in vitro angiogenesis.
Main Methods:
- Human umbilical vein endothelial cells (HUVECs) conditioned by PCa were used for in vitro assays.
- Bromodeoxyuridine (BrdU) assay for proliferation, wound healing assay for migration.
- Tube formation and spheroid sprouting assays for in vitro angiogenesis, Western blotting for ROCK activity (p-MYPT-1).
Main Results:
- Fasudil inhibited PCa-induced endothelial cell proliferation (100 µM) and migration (30 µM).
- Significant inhibition of in vitro angiogenesis: tube formation (>3 µM), spheroid sprout length/thickness (10-30 µM).
- Western blotting confirmed ROCK inhibition by fasudil (decreased p-MYPT-1 expression).
Conclusions:
- Fasudil demonstrates significant anti-angiogenic effects against PCa in vitro.
- Fasudil effectively targets endothelial cell proliferation, migration, and angiogenesis.
- Fasudil shows potential as a therapeutic anti-angiogenic agent for prostate cancer.
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