| Project/Area Number |
24792185
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Surgical dentistry
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| Research Institution | Niigata University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 口腔扁平上皮癌 / 上皮内癌 / keratin 17 / 14-3-3 sigma / siRNA / Keratin 17 |
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| Research Abstract |
We determined immunohistochemical profiles of 14-3-3 sigma and Keratin(K) 17 in tissue specimens of oral borderline malignancies and SCC as well as in ZK-1, an oral SCC cell line. In addition, to elucidate function of K17 in carcinoma cells, we examined cell proliferation and migration of ZK-1 cells when their K17 gene expressions were suppressed by knockdown using K17-siRNA (K17-siRNA cells). Both 14-3-3 sigma and K17 were similarly expressed in the cytoplasm of oral SCC and CIS cells but not in normal or dysplastic epithelia at tissue levels. They both were demonstrated in the cytoplasm of control ZK-1 cells, while 14-3-3 sigma was converted from the cytoplasm into the nucleus in K17-siRNA cells. The proliferation of K17-siRNA cells was significantly suppressed on day 4 after seeding. In addition, they migrated slower in scratch wound assays. The results indicate the K17 expression play an important role in promoting carcinoma cell growth in association with 14-3-3 sigma.
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