Study of the mechanism of cancer-risk increase due to diabetes and suggestion of the molecular-targeting cancer prevention for the cancer
| Project/Area Number |
16H05260
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Hygiene and public health
|
|---|
| Research Institution | Kyoto Prefectural University of Medicine |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2016-04-01 – 2019-03-31
|
| Project Status |
Completed (Fiscal Year 2018)
|
| Budget Amount *help |
¥16,510,000 (Direct Cost: ¥12,700,000、Indirect Cost: ¥3,810,000)
Fiscal Year 2018: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2017: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000)
Fiscal Year 2016: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
|
|---|
| Keywords | がん予防 / 糖尿病 / TRAIL / 癌予防 |
|---|
| Outline of Final Research Achievements |
TRAIL is a cytokine which can induce apoptosis against cancer cells, and contribute to cancer prevention. We have focused on TRAIL and examined whether the decline of immunity due to diabetes resulted in the down-regulation of TRAIL expression causing subsequent carcinogenesis and the up-regulation of leptin expression.
We compared the expression of TRAIL mRNA of the organ samples from a type 2 diabetes model of the mouse with those from the control mouse. As the results, TRAIL expressions of cDNA samples derived from lung of the diabetes model animals were lower than those from control mouse. Next, we showed the suppressive effect of leptin against the IFN-activated PBMCs to produce TRAIL. Furthermore, we focused on PED which were reported to be overexpressed in type 2 diabetes mellitus and mediate TRAIL resistance in human non-small cell lung cancer. Therefore, we tried the screening of the down-regulator of PED expression.
|
| Academic Significance and Societal Importance of the Research Achievements |
本邦では複数の疫学研究の結果から「日本人糖尿病患者の癌罹患リスク増大」が報告され、重大な社会的問題として取り上げられているが、その分子機序については現在も十分に明らかとされていない。本研究課題の成果は、癌予防に寄与するサイトカインであるTRAILの発現低下が、その一機序の説明になりうるかもしれないことを示している。研究代表者らが取り組んでいる、TRAIL経路の活性化による癌予防法の提案・応用に向けて、今回の研究成果が生かせられると考えている。
|
Report
(4 results)
Research Products
(7 results)
-
-
[Journal Article] The histone deacetylase inhibitor OBP-801 and eribulin synergistically inhibit the growth of triple-negative breast cancer cells with the suppression of survivin, Bcl-xL, and the MAPK pathway.2018
Author(s)
Ono H, Sowa Y, Horinaka M, Iizumi Y, Watanabe M, Morita M, Nishimoto E, Taguchi T, Sakai T.
-
Journal Title
Breast Cancer Research and Treatment
Volume: 171
Issue: 1
Pages: 43-52
DOI
Related Report
Peer Reviewed
-
-
-
-
-
