| Project/Area Number |
63570933
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
外科・放射線系歯学
|
|---|
| Research Institution | Tokyo Medical and Dental University |
|---|
Principal Investigator |
HORIKOSHI Masaru Tokyo Med. Staff and Dent. Univ., 歯学部, 助手 (00014283)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
RIKIMARU Koichi Tokyo Med. Staff and Dent. Univ., 歯学部, 助手 (40220800)
KUSAMA Mikio Tokyo Med. Staff and Dent. Univ., 歯学部, 助手 (60124690)
IWASA Toshiaki Tokyo Med. Staff and Dent. Univ., 歯学部, 助手 (10107302)
|
|---|
| Project Period (FY) |
1988 – 1989
|
| Project Status |
Completed (Fiscal Year 1989)
|
| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1989: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1988: ¥1,300,000 (Direct Cost: ¥1,300,000)
|
|---|
| Keywords | Oral Cancer / Sguamous cell carcinoma / human Epidermal growth factor / invasion model / Interleukin-1 / cytokine / Bone resorption / Parathyroid hormone related protein / インタ-ロイキン1 / 完全合成無蛋白培地 / IL-1 / DNA合成促進物質 / 無血清培養 / 細胞成長因子 |
|---|
| Research Abstract |
Squamous cell carcinoma (SCC)represents about 90% of total oral cancers. It was reported that the growth of SCC cells was inhibited by epidermal growth factor (EGF) at the dose which is stimulatory for the growth of other type of cancer cells. In this project it was revealed that the third disulfide loop from N-terminal of human EGF was very important for their growth suppressive function. To investigate on the possibility of the usage of EGF for the treatment of SCC, further studies, such as in vivo study using nude mice, should be carried out.
An in vitro model was developed to study the mechanisms of invasion in oral cancer, where SCC cells were cultured on the particular matrix consisting of collagen gel and human living fibroblasts. This model demonstrated that fibroblasts was implicated in the invasion in SCC cells in vitro, and each cell line presented the similar pattern of invasion as observed in original tumor specimen.
Furthermore, we developed a novel protein-free medium, designated PF86-1, for the culture of SCC cells. Since the protein-free culture system using PF86-1 seems to have significant advantage for the study on the tumor products, which may be implicated in the clinical behavior of tumor cells, we attempted to identify the bioactive substances secreted by SCC cells into the culture medium. In the study, it was shown that although SCC cells produced IL-1alpha and IL-1beta, only IL-1alpha was secreted into culture medium and IL-1beta was retained in the cytoplasm. Further study revealed that IL-1alpha might be an important factor causing hypercalcemia in SCC. Patients via its bone resorbing activity, as suggested by the result that IL-1alpha produced by SCC cells promoted the release of ^<45>Ca from the pre-labeled mouse calvariae in vitro.
|
