| Project/Area Number |
24390385
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
TAKAHARA Miki 旭川医科大学, 医学部, 講師 (50322904)
KISHIBE Kan 旭川医科大学, 医学部, 助教 (80447101)
KOBAYASHI Hiroya 旭川医科大学, 医学部, 教授 (90280867)
UEDA Seigo 旭川医科大学, 医学部, 助教 (90447102)
NAGATO Toshihiro 旭川医科大学, 医学部, 助教 (80431419)
KOMABAYASHI Yuki 旭川医科大学, 医学部, 助教 (40548864)
熊井 琢美 旭川医科大学, 医学部, 助教 (00596306)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥18,330,000 (Direct Cost: ¥14,100,000、Indirect Cost: ¥4,230,000)
Fiscal Year 2014: ¥5,720,000 (Direct Cost: ¥4,400,000、Indirect Cost: ¥1,320,000)
Fiscal Year 2013: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2012: ¥6,630,000 (Direct Cost: ¥5,100,000、Indirect Cost: ¥1,530,000)
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| Keywords | 鼻性NK/T細胞リンパ腫 / Epstein-Barr virus / LMP1 / CD70 / chemokine / CCR4 / miR-15a / 頭頸部外科学 / 悪性リンパ腫 / 悪性腫瘍 |
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| Outline of Final Research Achievements |
Nasal natural killer/T cell lymphoma (NNKTL) is Epstein-Barr virus (EBV)-associated malignancy and characterized by a poor prognosis. In the present study, we found that CD70 was specifically expressed in NNKL cell lines and that it played a role in cell growth by binding to soluble CD27. Moreover, we found that CCL17 and CCL22 was upregulated in NNKTL cell lines and CCR4 was observed on NNKTL cell lines. In addition, we showed that anti-CD70 and anti-CCR4 antibodies could induce complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) against NKKTL cells, respectively. Furthermore, we revealed that microRNA (miR)-15a was downregulated in NNKTL cell lines and that miR-15a led to decreased expression of MYB and cyclin D1, thereby resulting in inhibition of cell proliferation.
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