Identification of molecular basis of NK/T cell lymphoma by using proteomics
Project/Area Number |
25460436
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Human pathology
|
Research Institution | Osaka University |
Principal Investigator |
HONMA KEIICHIRO 大阪大学, 医学(系)研究科(研究院), 助教 (20505945)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | NK/T細胞リンパ腫 / 悪性リンパ腫 |
Outline of Final Research Achievements |
We conducted quantitative proteomics analysis by iTRAQ. Marked quantitative differences were observed in the four proteins in NK/T cell lymphoma cell lines compare to the control NK cells introducing EBV genes.Concordance of protein expression pattern was observed in one protein (DFCP1) between NK/T cell lymphoma clinical samples and normal NK cell samples by using immunohistochemical analysis. Induction of clonogenicity by DFCP1 and cellular apoptosis by knockdown of DFCP1 was observed in the NK lymphoma cell line and NK cells intrducing EBV genes, whereas DFCP1 was no effect in cellular survival and proliferation in control NK cells. Next we analysed cooperative interactions of DFCP1 and EBV genes using large-scale proteome analysis co-immunoprecipitation coupled to mass spectrometry. We identified the interaction of DCFP with EBV gene A73. These results revealed that DFCP1 may play an imortant role in NK lymphomagenesis.
|
Report
(4 results)
Research Products
(2 results)