Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 108, Issue 5, Pages 1897-1902Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1019059108
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Funding
- Shanghai Municipal Committee of Science and Technology [06dj14002, 09XD1403000]
- National Scientific Foundation of China [30871108]
- Chinese National Key Basic Research Project 973 [2007CB947800, 2010CB945600]
- E-Institutes of Shanghai Municipal Education Commission [E03003]
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RA-inducible gene I (RIG-I/DDX58) has been shown to activate IFN-beta 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-alpha 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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