A role of activated Sonic hedgehog signaling for the cellular proliferation of oral squamous cell carcinoma cell line

Sonic hedgehog (Shh) is a secreted morphogen crucial for appropriate cellular proliferation during mammalian development. The activated Shh signaling is known to predispose to human tumors such as medulloblastoma and basal cell carcinoma, while a role of Shh signaling in the other common tumors is s...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2004-02, Vol.314 (2), p.313-320
Main Authors: Nishimaki, Haruaki, Kasai, Kenji, Kozaki, Ken-ichi, Takeo, Tomohiro, Ikeda, Hiroshi, Saga, Shinsuke, Nitta, Masakazu, Itoh, Gen
Format: Article
Language:English
Subjects:
Amides - pharmacology
Apoptosis
Blotting, Western
Carcinoma, Squamous Cell - metabolism
Cell Cycle
Cell Division
Cell Line, Tumor
Cell Separation
Culture Media, Conditioned - pharmacology
Cyclopamine
Dose-Response Relationship, Drug
Enzyme Inhibitors - pharmacology
Flow Cytometry
G1 Phase
Hedgehog Proteins
Humans
Intracellular Signaling Peptides and Proteins
Mouth Neoplasms - metabolism
Oral cancer
Protein-Serine-Threonine Kinases - metabolism
Pyridines - pharmacology
Rho-associated kinase
rho-Associated Kinases
S Phase
Signal Transduction
Smoothened
Sonic hedgehog
Squamous cell carcinoma
Time Factors
Trans-Activators - metabolism
Veratrum Alkaloids - pharmacology
Y-27632
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Summary:Sonic hedgehog (Shh) is a secreted morphogen crucial for appropriate cellular proliferation during mammalian development. The activated Shh signaling is known to predispose to human tumors such as medulloblastoma and basal cell carcinoma, while a role of Shh signaling in the other common tumors is still controversial. Here we showed the overexpression of Shh in five cell lines among 14 human oral squamous cell carcinoma (OSCC) cell lines. One of the Shh-expressing OSCC cell lines HSQ-89 showed the inhibition of G1/S transition and apoptotic cell death by treatment with Cyclopamine, a steroidal alkaloid that blocks the intracellular Shh signaling. Furthermore, we found that treatment with Y-27632, a specific inhibitor of Rho-associated kinase, mimicked the effect of Cyclopamine on the cell cycle progression of HSQ-89. Our study revealed the involvement of activated Shh signaling in the cellular proliferation of OSCC cells, indicating Shh signaling might be a good therapeutic target for OSCC.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2003.12.097