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RIG-I modulates Src-mediated AKT activation to restrain leukemic stemness.

Xian-Yang Li1, Lin-Jia Jiang1, Lei Chen1

  • 1State Key Laboratory for Medical Genomics and Shanghai Institute of Hematology, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, People's Republic of China; Shanghai E-Institute for Model Organisms, Shanghai 200025, People's Republic of China.

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Retinoic acid-inducible gene I (RIG-I) inhibits leukemia cell growth by blocking the Src/AKT pathway in acute myeloid leukemia (AML). This discovery offers new insights into RIG-I

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Immunology

Background:

  • Retinoic acid (RA)-inducible gene I (RIG-I) is upregulated during RA-induced acute myeloid leukemia (AML) maturation.
  • The precise role of RIG-I in maintaining AML's leukemogenic potential remains unclear.

Purpose of the Study:

  • To elucidate the mechanism by which RIG-I influences AML cell signaling.
  • To investigate the biological relevance of RIG-I expression in AML pathogenesis.

Main Methods:

  • Investigated RIG-I's effect on AKT-mTOR signaling in AML cells.
  • Analyzed RIG-I's interaction with Src family kinases and AKT pathway components.
  • Utilized site-directed mutagenesis of the RIG-I PxxP motif.
  • Assessed the impact of RIG-I modulation on AML cell proliferation and in vivo repopulating capacity.

Main Results:

  • RIG-I inhibits Src-facilitated AKT-mTOR activation in AML cells independently of foreign RNA.
  • Reduced RIG-I expression leads to hyperactivity of Src family kinases, promoting AKT activation in primary AML blasts.
  • A PxxP motif in RIG-I competitively inhibits the Src/AKT association by interacting with the Src SH3 domain.
  • Mutating the RIG-I PxxP motif abrogates its inhibitory effects on AKT activation, cell proliferation, and leukemia cell repopulation.

Conclusions:

  • RIG-I possesses intrinsic antileukemia activity by competitively inhibiting the Src/AKT signaling axis.
  • Targeting the RIG-I-Src/AKT interaction could represent a novel therapeutic strategy for AML.