| Project/Area Number |
17591344
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Iwate Medical University |
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Principal Investigator |
OGASAWARA Satoshi Iwate Med. Univ., School of Med., Dept. of Surg., Research Associate, 医学部, 助手 (40326658)
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| Co-Investigator(Kenkyū-buntansha) |
MAESAWA Chihaya Iwate Med. Univ., School of Med., Dept. of Pathol., Associate Prof., 医学部, 助教授 (10326647)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2005: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | anaplastic thyroid cancer / cell cycle / Chk1 / UCN-01 / apoptosis / papillary thyroid cancer / ATP assay / 甲状腺未分化癌 |
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| Research Abstract |
Anaplastic thyroid cancer (ATC) has an even worse prognosis, and they have not cured by the surgery with a very low chance of surviving from the disease. Tb develop a new strategy for the treatment of ATC, we examine Chk1 inhibitor (UCN-01) in ATC cell lines.
We determined expression and/or phosphorylation status of ART, ATM, and Chk1 in ATC cell lines using Western blotting. Proliferation activities were measured by ATP assays.
Marked repression and apoptosis was observed in ATC cells after the treatment with UCN-01, in dose- and time dependent manner. Furthermore, we confirmed down-regulation of ART, ATM, and Chk1 phosphorylation. MiR-138 was significantly down-regulated in ATC cell lines in comparison with papillary thyroid cancer cell lines. Its loss of miR-138 was closely associated with Chk1 status in ATC cell lines.
Our preclinical trials suggested that UCN-01 was useful for the management of ATC patients, and the miR-138 expression might regulate the Chk1 phosphorylation status.
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