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

Linjia Jiang(Shanghai Institute of Hematology), Nannan Zhang(Shanghai Institute of Hematology), Fei Ding(Shanghai Institute of Hematology), Xian-Yang Li(Shanghai Institute of Hematology), Lei Chen(Shanghai Institute of Hematology), Hongxin Zhang(Shanghai Jiao Tong University), Wu Zhang(Shanghai Institute of Hematology), Sai‐Juan Chen(Shanghai Institute of Hematology), Zhugang Wang(Shanghai Jiao Tong University), Junmin Li(Shanghai Institute of Hematology), Zhu Chen(Shanghai Institute of Hematology), Jiang Zhu(Shanghai Institute of Hematology)
Proceedings of the National Academy of Sciences
January 11, 2011
Cited by 81Open Access
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Abstract

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.


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