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RA-inducible gene-I induction augments STAT1 activation to inhibit leukemia cell proliferation

2011; National Academy of Sciences; Volume: 108; Issue: 5 Linguagem: Inglês

10.1073/pnas.1019059108

1091-6490

Linjia Jiang, Nannan Zhang, Fei Ding, Xian-Yang Li, Lei Chen, Hongxin Zhang, Wu Zhang, Sai‐Juan Chen, Zhugang Wang, Junmin Li, Zhu Chen, Jiang Zhu,

Immune Cell Function and Interaction

RA-inducible gene I (RIG-I/DDX58) has been shown to activate IFN-β promoter stimulator 1 (IPS-1) on recognizing cytoplasmic viral RNAs. It is unclear how RIG-I functions within the IFN and/or RA signaling process in acute myeloid leukemia (AML) cells, however, where obvious RIG-I induction is observed. Here, we show that the RIG-I induction functionally contributes to IFN-α plus RA-triggered growth inhibition of AML cells. Interestingly, although RIG-I induction itself is under the regulation of STAT1, a major IFN intracellular signal mediator, under circumstances in which it does not stimulate IPS-1, it conversely augments STAT1 activation to induce IFN-stimulatory gene expression and inhibit leukemia cell proliferation. Thus, our results unveil a previously undescribed RIG-I activity in regulating the cellular proliferation of leukemia cells via STAT1, which is independent of its classic role of sensing viral invasion to trigger type I IFN transcription.