期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 286, 期 14, 页码 -出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M110.159756
关键词
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资金
- Korean government (Ministry of Education & Science Technology) [R11-2005-017-05003-0, 10033778]
- Korea Evaluation Institute of Industrial Technology (KEIT) [10033778] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
IL-32 was recently identified as a proinflammatory cytokine that is induced by IL-18 in natural killer (NK) cells and is highly correlated with inflammatory disorders. However, the relationship between IL-32 and tumor progression is still unknown. In this study, we investigated whether overexpression of IL-32 affects susceptibility of chronic myeloid leukemia (CML) cells to NK cells. Interestingly, IL-32 alpha-overexpressing CML cell lines, K562, Kcl22, and BV173, showed higher NK cell-mediated killing. Flow cytometry analysis revealed that overexpression of IL-32 alpha induced increased expression of Fas and UL16-binding protein 2 (ULBP2) in CML cells. The direct relationship between overexpression of surface molecules by IL-32 alpha and increased NK cell-mediated killing was confirmed by Fas or ULBP2 siRNA transfection. IL-32 alpha-induced Fas and ULBP2 expression are regulated p38 MAPK. In addition, the transcription factor Ets1 plays a key role in ULBP2 specific expression by IL-32 alpha overexpression in ULBP family members. Taken together, these data show that IL-32 alpha stimulates Fas and ULBP2 expression via activation of p38 MAPK, which increases NK susceptibility of CML cells. Enhanced NK cell susceptibility of CML cells by IL-32 alpha overexpression may improve the efficiency of NK cell-based immunotherapy.
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