| Project/Area Number |
16K20559
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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 | Chiba University |
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Principal Investigator |
KOIKE KAZUYUKI 千葉大学, 大学院医学研究院, 特任助教 (10618060)
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| Project Period (FY) |
2016-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | α1β1インテグリン / Semaphorin7A / 口腔扁平上皮癌 / microarray / 増殖抑制法 / Semaphorin 7A / α1β1 インテグリン / 口腔癌 |
|---|
| Outline of Final Research Achievements |
Significant SEMA7A upregulation was detected in the cell lines and most primary OSCCs compared with the normal counterparts. The SEMA7A expression level was correlated closely with tumoral size and metastasis. In vitro, cellular growth, migration, and invasion in SEMA7A knockdown cells significantly decreased with inactivated extracellular regulated kinase (ERK), and cell-cycle arrest at the G1 phase resulting from upregulation of the cyclin-dependent kinase inhibitors, including p21Cip1 and p27Kip1. These data indicated that SEMA7A may play a role in OSCCs via MAPK signaling cascades, making it a potentially useful diagnostic/therapeutic target for use in patients with OSCC.
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