Abstract：
:Acute myeloid leukemia (AML) cells in vivo are constantly exposed to lymphangiogenic cytokines such as VEGF-C. However, it is poorly understood how the VEGF-C signaling modulates the immune functions in the tumor microenvironment. We have previously reported that natural killer (NK) cells in AML patients strongly upregulated VEGFR-3, the major VEGF-C receptor, and that the VEGFR-3 expression level in NK cells inversely correlates with their cytotoxic potential. These findings have led us to hypothesize that VEGFR-3 inhibition may reinstate the cytotoxic capacity of the AML-associated NK cells. To address this hypothesis, we employed a pharmaceutical approach to block the VEGFR-3 function in the murine model of syngeneic myelogenous leukemia. Using various molecular and cellular analyses, we assessed the correlation between VEGFR-3 inhibition and NK cell cytotoxicity. Indeed, we found that leukemic environment is highly enriched with lymphangiogenic stimuli, and that VEGFR-3 inhibition restored NK cell killing function with an increased IFN-γ level, providing a therapeutic implication of VEGFR-3 against AML. Together, we demonstrate the therapeutic value of functional modulation of NK cells by blocking VEGFR-3, and provide a possibility of advanced therapeutic approaches using immune cells against myelogenous leukemia.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Lee JY,Park S,Min WS,Kim HJdoi
10.1016/j.canlet.2014.08.027subject
Has Abstractpub_date
2014-11-28 00:00:00pages
281-9issue
2eissn
0304-3835issn
1872-7980pii
S0304-3835(14)00467-4journal_volume
354pub_type
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