| Project/Area Number |
15K18414
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Tumor biology
|
|---|
| Research Institution | University of the Ryukyus |
|---|
Principal Investigator |
ISHIKAWA Chie 琉球大学, 亜熱帯島嶼科学超域研究推進機構, 助教 (90542358)
|
|---|
| Project Period (FY) |
2015-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2015: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
|
|---|
| Keywords | 成人T細胞白血病（ATL） / HTLV-1 / ISL-1 / Tax / c-myc / 成人T細胞白血病 |
|---|
| Outline of Final Research Achievements |
HTLV-1 is the etiological agent of adult T-cell leukemia (ATL). Although the viral protein Tax plays crucial roles for the development of ATL, the underlying mechanisms remain obscure. ISL-1, LIM homeodomain transcription factor, is specifically expressed in certain tissue types only. Recently, ISL-1 is suggested to play an oncogenic role. The expression of ISL-1 was assessed in 8 HTLV-1-infected T-cell lines and 3 uninfected T-cell lines. RT-PCR results demonstrated a marked highly expression of ISL-1 mRNA in 5 HTLV-1-infected T-cell lines. The expression levels of ISL-1 mRNA were associated with those of Tax mRNA. ISL-1 protein was also detected in 3 Tax-positive HTLV-1-infected T-cell lines. HTLV-1 infection and Tax overexpression induced the expression of ISL-1 in T cells. Notably, ISL-1 overexpression promoted T-cell proliferation. Furthermore, ISL-1 activated the expression of c-myc. Our results provide insights into the new relationships between ISL-1 and HTLV-1 oncogenesis.
|
