| Literature DB >> 25038230 |
Gregory J Baker1, Peter Chockley1, Viveka Nand Yadav1, Robert Doherty1, Michael Ritt2, Sivaraj Sivaramakrishnan3, Maria G Castro1, Pedro R Lowenstein4.
Abstract
Natural killer (NK) cells safeguard against early tumor formation by destroying transformed target cells in a process referred to as NK immune surveillance. However, the immune escape mechanisms used by malignant brain tumors to subvert this innate type of immune surveillance remain unclear. Here we show that malignant glioma cells suppress NK immune surveillance by overexpressing the β-galactoside-binding lectin galectin-1. Conversely, galectin-1-deficient glioma cells could be eradicated by host NK cells before the initiation of an antitumor T-cell response. In vitro experiments demonstrated that galectin-1-deficient GL26-Cit glioma cells are ∼3-fold more sensitive to NK-mediated tumor lysis than galectin-1-expressing cells. Our findings suggest that galectin-1 suppression in human glioma could improve patient survival by restoring NK immune surveillance that can eradicate glioma cells. Cancer Res; 74(18); 5079-90. ©2014 AACR. ©2014 American Association for Cancer Research.Entities:
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Year: 2014 PMID: 25038230 PMCID: PMC4184887 DOI: 10.1158/0008-5472.CAN-14-1203
Source DB: PubMed Journal: Cancer Res ISSN: 0008-5472 Impact factor: 12.701