2019 Fiscal Year Final Research Report
Molecular analysis of ameloblastoma exacerbation factor for development of new therapeutic agents
| Project/Area Number |
17K17286
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Surgical dentistry
|
|---|
| Research Institution | Iwate Medical University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2017-04-01 – 2020-03-31
|
| Keywords | エナメル上皮腫 / 歯周病原細菌 / 酪酸 |
|---|
| Outline of Final Research Achievements |
It was suggested that Laminin332 is involved in subepithelial infiltration of ameloblastoma.
In addition, the possibility was considered that butyric acid produced by oral bacteria, especially periodontopathic bacteria, stimulates the production of EGF and TGFβ1 from ameloblastoma, and these cytokines increase the expression of Laminin332 involved in invasion by acting on autocrine ameloblastoma.
Therefore, it was suggested that local control of butyric acid-producing bacteria is very important in the infiltration (malignant transformation) of ameloblastoma.
|
| Free Research Field |
口腔微生物学
|
| Academic Significance and Societal Importance of the Research Achievements |
エナメル上皮腫の顎骨内の侵襲的な増大や，まれに見られる悪性化・転移には，増悪因子としてLaminin等の発現や，サイトカインの関与が示唆されてきた．しかし，腫瘍の部位により細胞に多様性のある本疾患の悪性化に関わるメカニズムについては不明な点が多かった．さらに，その増悪には歯周病原細菌の関与が疑われるものの，それらの影響はこれまで全く検討されていなかった．本研究では，同一のエナメル上皮腫組織から樹立された新たな3種の細胞株を用い，細胞接着因子，サイトカインに加え，細菌由来因子も含めた本疾患の増悪に関するメカニズムを分子生物学的観点から明らかにしたことで，新規治療薬開発の一助となると考えられる．
|
