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Bradykinin-induced Ca2+ signaling in human oral squamous cell carcinoma HSC-3 cells
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- Authors
- Issue Date
- 2009
- Publisher
- The Korean Academy of Oral Biology
- Citation
- International Journal of Oral Biology 2009;34:73-79
- Keywords
- Bradykinin ; oral squamous cell carcinoma ; HSC-3 cells ; phospholipase C
- Abstract
- Cytosolic Ca
2+ is an important regulator of tumor cell
proliferation and metastasis. Recently, the strategy of
blocking receptors and channels specific to certain cancer
cell types has emerged as a potentially viable future
treatment. Oral squamous cell carcinoma is an aggressive
form of cancer with a high metastasis rate but the receptormechanisms
involved in Ca
2+ signaling in these tumors have
not yet been elucidated. In our present study, we report that
bradykinin induces Ca
2+
signaling and its modulation in the
human oral squamous carcinoma cell line, HSC-3.
Bradykinin was found to increase the cytosolic Ca
2+ levels in
a concentration-dependent manner. This increase was
inhibited by pretreatment with the phospholipase C-β
inhibitor, U73122, and also by 2-aminoethoxydiphenyl
borate, an inhibitor of the inositol 1,4,5-trisphosphate
receptor. Pretreatment with extracellular ATP also inhibited
the peak bradykinin-induced Ca
2+ rise. In contrast, the
ATP-induced rise in cytosolic Ca
2+ was not affected by
pretreatment with bradykinin. Pretreatment of the cells
with either forskolin or phorbol 12-myristate 13-acetate
(activators of adenylyl cyclase and protein kinase C,
respectively) prior to bradykinin application accelerated
the recovery of cytosolic Ca
2+ to baseline levels. These data
suggest that bradykinin receptors are functional in Ca
2+
signaling in HSC-3 cells and may therefore represent a
future target in treatment strategies for human oral
squamous cell carcinoma.
- ISSN
- 1226-7155
- Language
- English
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