PT - JOURNAL ARTICLE AU - KURODA, HIROMASA AU - KURIO, NAITO AU - SHIMO, TSUYOSHI AU - MATSUMOTO, KENICHI AU - MASUI, MASANORI AU - TAKABATAKE, KIYOFUMI AU - OKUI, TATSUO AU - IBARAGI, SOICHIRO AU - KUNISADA, YUKI AU - OBATA, KYOICHI AU - YOSHIOKA, NORIE AU - KISHIMOTO, KOJI AU - NAGATSUKA, HITOSHI AU - SASAKI, AKIRA TI - Oral Squamous Cell Carcinoma-derived Sonic Hedgehog Promotes Angiogenesis DP - 2017 Dec 01 TA - Anticancer Research PG - 6731--6737 VI - 37 IP - 12 4099 - http://ar.iiarjournals.org/content/37/12/6731.short 4100 - http://ar.iiarjournals.org/content/37/12/6731.full SO - Anticancer Res2017 Dec 01; 37 AB - Background: Sonic hedgehog (SHH) signaling is related to the pathogenesis of oral squamous cell carcinoma (OSCC), but its role in OSCC is not yet well understood. In this study, we analyzed the role of SHH signaling in OSCC. Materials and Methods: We examined the expression pattern of SHH and its signal proteins in clinically resected OSCC samples by immunohistochemistry. We also evaluated the function of SHH signaling using the hedgehog signaling inhibitor cyclopamine in vivo and in vitro by proliferation, migration and angiogenesis analyses. Results: We found that SHH was highly expressed in human tongue OSCC, whereas patched (PTCH1), glioma-associated oncogene 1 (GLI1) and GLI2 proteins were expressed in the microvascular cells in the tumor invasive front. Administration of cyclopamine to mice suppressed the growth and angiogenesis of OSCC xenografts in vivo. Moreover, cyclopamine inhibited endothelial cell proliferation and migration, and reduced aorta vascular length in the rat. Conclusion: These findings suggest that OSCC-derived SHH stimulates angiogenesis at the tumor invasive front.