| Project/Area Number |
21592199
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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 |
Otorhinolaryngology
|
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| Research Institution | Oita University |
|---|
Principal Investigator |
NOMI Nozomi 大分大学, 医学部, 助教 (40468020)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Masashi 大分大学, 医学部, 教授 (60211314)
WATANABE Tetsuo 大分大学, 医学部, 准教授 (50231709)
HIRANO Takashi 大分大学, 医学部, 講師 (20305056)
KODAMA Satoru 大分大学, 医学部, 講師 (40325717)
|
|---|
| Project Period (FY) |
2009 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
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| Keywords | 頭頸部癌 / 腫瘍免疫 / TLR / TLR2 / アポトーシス / 細胞増殖 |
|---|
| Research Abstract |
The innate immune system builds up the host defense against a huge diversity of pathogens like viruses, bacteria and fungi. Toll-like receptors(TLRs) are one of the pattern recognition receptors(PRRs), which trigger the initiation of various defense mechanisms. The expression of TLRs represents an important link between innate and adaptive immune responses. Recently, the expression of TLRs in several cancer cells has been reported, however, the exact roles of TLRs in cancers are still unclear. In this study, we investigated the expressions of TLRs and its signaling in human head and neck squamous cell carcinomas(HNSCCs). The expressions of TLRs in 8 HNSCC cell lines were examined. Cells were incubated with Pam3CSK4 and polyI : C, and viability of cells was tested with MTT assay. TLR2 and TLR3 were widely expressed in human HNSCCs. Interestingly, the stimulation of TLR2 by Pam3cysSK4 induced cell proliferation, in a contrasting situation, the stimulation of TLR3 by poly I : C induced the apoptosis in cancer cells, both in dose-dependent manner. We also revealed that the stimulation of TLR2 might induce cell migration. In the present study, we demonstrated the proliferative activity of TLR2 and the proapoptotic activity of TLR3 expressed by HNSCCs. These results suggested that TLR2 and TLR3 could be the new target for therapy in HNSCCs.
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