Int J Oral Biol.
2014 Mar;39(1):1-7.
A Neuromedin B Receptor Blockade Inhibits the Growth of Human Oral Cancer Cells
- Affiliations
-
- 1Department of Oral Physiology, School of Dentistry, Pusan National University, Yangsan 626-870, South Korea. mkbae@pusan.ac.kr
- 2Department of Dental Pharmacology, School of Dentistry, Pusan National University, Yangsan 626-870, South Korea.
- 3Department of Oral Pathology, School of Dentistry, Pusan National University, Yangsan 626-870, South Korea.
- 4Department of Oral and Maxillofacial Surgery, School of Dentistry, Pusan National University, Yangsan 626-870, South Korea.
Abstract
- Neuromedin B (NMB) acts as a growth factor or a morphogen and plays a role in cancer progression. Indeed, the NMB receptor (NMB-R) is overexpressed in different types of tumors. In our current study, we investigated the involvement of NMB-R in the proliferation of oral cancer cells. Human oral squamous cell carcinoma (SCC) and human oral cancer cells, SCC-25 cells were found to be NMB-R-positive. The NMB-R antagonist PD168368 inhibited the proliferation of SCC-25 cells and reduced their colony formation capacity. We also found that PD168368 induced the cell cycle arrest and apoptosis of SCC-25 cells in a dose-/time-dependent manner. Overall, this antitumor activity of PD168368 in human oral cancer cells suggests that NMB-R is a potential target for the future prevention and treatment of human cancers.
- Full Text Links
-
- Actions
-
Cited
- CITED
-
- Close
- Share
-
- Similar articles
-
- Zerumbone, Sesquiterpene Photochemical from Ginger, Inhibits Angiogenesis
- An experimental study on the stimulatory effects of epidermal growth factor and transforming growth factor-alpha on the growth of squamous cancer cell lines
- Effect of intracelluar cyclic AMP on EGF receptor binding in human gastric adenocarcinoma cells
- Prognostic significance of epidermal growth factor receptor expression in human gastric carcinoma
- The Apoptotic Effect of the Hexane Extract of Rheum undulatum L. in Oral Cancer Cells through the Down-regulation of Specificity Protein 1 and Survivin
