Project/Area Number |
16K15202
|
Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
Allocation Type | Multi-year Fund |
Research Field |
General pharmacology
|
Research Institution | Osaka University |
Principal Investigator |
Nishikawa Keizo 大阪大学, 免疫学フロンティア研究センター, 特任准教授(常勤) (30516290)
|
Project Period (FY) |
2016-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2017: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | Osteoclast / DNA methylation / Dnmt3a / Epigenetics / metastasis / Bone / Cancer / がん / 破骨細胞 / 骨転移 / エピゲノム創薬 / エピジェネティクス / DNAメチル化 / 創薬 |
Outline of Final Research Achievements |
We recently demonstrated that a novel inhibitor of DNA methylation, TF3, has the inhibitory effect on osteoclast differentiation, and further demonstrated that TF3 is a promising drug candidate for the treatment of osteoporosis. Several cancers that metastasize to bone negatively perturb the remodeling process through a series of interactions with osteoclasts. These interactions have been described as the "vicious cycle" of cancer metastasis in bone. In this study, we investigated the effect of perturbation of osteoclastogenesis by TF3 on cancer bone metastasis. An experimental bone metastasis model was developed by injecting mice with murine melanoma B16BL6 cells. Using the mice model, we found that TF3 has the inhibitory effect on B16BL6 cell metastasis in bone. These results suggest that TF3 is a promising drug candidate for cancer bone metastasis.
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