A foundational study for targeted therapy against EB virus and tumor growth factor in nasal NK/T-cell lymphoma

2014 Fiscal Year Final Research Report

• Project/Area Number: 24390385
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Otorhinolaryngology
• Research Institution: Asahikawa Medical College
• Principal Investigator: HARABUCHI Yasuaki 旭川医科大学, 医学部, 教授 (80208686)
• 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)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 鼻性NK/T細胞リンパ腫 / Epstein-Barr virus / LMP1 / CD70 / chemokine / CCR4 / miR-15a

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.

Free Research Field

医歯薬学