Cancers | |
Loss of STAT3 in Lymphoma Relaxes NK Cell-Mediated Tumor Surveillance | |
Eva Maria Putz1  Maria Agnes Hoelzl2  Julia Baeck1  Zsuzsanna Bago-Horvath1  Christian Schuster2  Brian Reichholf1  Daniela Kern3  Fritz Aberger3  Veronika Sexl1  | |
[1] Institute of Pharmacology and Toxicology, University of Veterinary Medicine, Veterinaerplatz 1, Vienna 1210, Austria; E-Mails:;Institute of Pharmacology, Center for Physiology and Pharmacology, Medical University of Vienna (MUV), Waehringer Strasse 13A, Vienna 1090, Austria; E-Mails:;Department of Molecular Biology, University of Salzburg, Hellbrunnerstrasse 34, Salzburg 5020, Austria; E-Mails: | |
关键词: STAT3; lymphoma; BCR/ABL; NK cells; tumor immune surveillance; | |
DOI : 10.3390/cancers6010193 | |
来源: mdpi | |
【 摘 要 】
The transcription factors and proto-oncogenes STAT3 and STAT5 are highly activated in hematological malignancies and represent promising therapeutic targets. Whereas the importance of STAT5 as tumor promoter is beyond doubt, the role of STAT3 in hematological cancers is less well understood. Both, enforced as well as attenuated expression of STAT3 were reported in hematopoietic malignancies. Recent evidence implicates STAT3 as key player for tumor immune surveillance as it both mediates the production of and response to inflammatory cytokines. Here we investigated the effects of STAT3 deletion in a BCR/ABL-induced lymphoma model, which is tightly controlled by natural killer (NK) cells
【 授权许可】
CC BY
© 2014 by the authors; licensee MDPI, Basel, Switzerland.
【 预 览 】
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RO202003190029829ZK.pdf | 763KB | download |