CDK8-mediated STAT1-S727 phosphorylation restrains NK cell cytotoxicity and tumor surveillance

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Abstract

The transcription factor STAT1 is important in natural killer (NK) cells, which provide immediate defense against tumor and virally infected cells. We show that mutation of a single phosphorylation site (. Stat1-S727A) enhances NK cell cytotoxicity against a range of tumor cells, accompanied by increased expression of perforin and granzyme B. Stat1-S727A mice display significantly delayed disease onset in NK cell-surveilled tumor models including melanoma, leukemia, and metastasizing breast cancer. Constitutive phosphorylation of S727 depends on cyclin-dependent kinase 8 (CDK8). Inhibition of CDK8-mediated STAT1-S727 phosphorylation may thus represent a therapeutic strategy for stimulating NK cell-mediated tumor surveillance

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Putz, E. M., Gotthardt, D., Hoermann, G., Csiszar, A., Wirth, S., Berger, A., … Sexl, V. (2013). CDK8-mediated STAT1-S727 phosphorylation restrains NK cell cytotoxicity and tumor surveillance. Cell Reports, 4(3), 437–444. https://doi.org/10.1016/j.celrep.2013.07.012

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