| Project/Area Number |
07671965
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Niigata University |
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Principal Investigator |
CHENG Jun Niigata Univ.School of Dentistry, Assistant Professor, 歯学部, 助手 (40207460)
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| Co-Investigator(Kenkyū-buntansha) |
SAKU Takashi Niigata Univ.School of Dentistry, Professor, 歯学部, 教授 (40145264)
KIMURA Shin Niigata Univ.School of Dentistry, Assistant Professor, 歯学部, 助手 (80251825)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1996: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1995: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | salivary gland tumor / adenoid cystic carcinoma / three-dimensional culture / extracellular matrix / type III collagen / type IV collagen / heparan sulfate proteoglycan / fibronectin |
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| Research Abstract |
Adenoid cystic carcinoma is histologically characterized by a cribriform appearance that results from formation of multi-pseudocystic spaces in each tumor cell nest. The pseudocysts are surrounded by tumor cells and are filled with extracellular matrix components such as basement membrane molecules. We have demonstrated that these basement membrane molecules were produced by ACC2 and ACC3 cells, established independently from human salivary adenoid cystic carcinomas.
The retention of abundant basement membrane molecules in the stromal space that includes pseudocystic cavities suggests that basement membrane matrix is essential for proliferation of adenoid cystic carcinoma cells. We have proposed that their frequent invasion of peripheral nerves, blood vessels, and skeletal muscles can be interpreted to mean that adenoid cystic carcinoma cells have an affinity for basement membranes. We have also shown that adenoid cystic carcinoma dells attach, spread, and grow rapidly on matrices conta
… More
ining basement membrane molecules, using ACC3 cells of human adenoid cystic carcinoma origin. However, it is still unknown how pseudocysts are formed and why these particular structures are commonly associated with their growth. Thus, we planned to establish a three-dimension-culture system of adenoid cystic carcinoma cells in which the tumor nest architecture could be analyzed in a longer period than a monolayr culture system. In this study, we successfully cultured ACC cells in collagen gel and examined the process of pseudocyst formation in tumor cell colonies. At the same time, we examined xenografts of ACC2 in SCID mice and compared the nature of pseudocystic spaces formed in the transplants with that in the collagen gel cultures. In the collagen gel culture, the cells formed spherical colonies and the tumor cell nests contained vacuolar structures that were immunopositive for heparan sulfate proteoglycan, type III collagen and type IV collagen, and fibronectin. Transplants of ACC2 cells in SCID mice grew to form tumor messes in which pseudocysts were formed. The results indicate that our collagen gel culture system provides physiological conditions for ACC2 cells to secrete particular extracelluar matrix molecules and form pseudocystic spaces. Less
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