2. Academic Validation
  3. Acute myeloid leukemia cell-derived extracellular vesicles carrying microRNA-548ac regulate hematopoietic function via the TRIM28/STAT3 pathway

Acute myeloid leukemia cell-derived extracellular vesicles carrying microRNA-548ac regulate hematopoietic function via the TRIM28/STAT3 pathway

  • Cancer Gene Ther. 2022 Jul;29(7):918-929. doi: 10.1038/s41417-021-00378-6.
Chen Zhao  # 1,  Yang Zhao  # 2,  Jiaqi Zhao 3,  Guixian Meng 4,  Shuyu Huang 4,  Yichen Liu 4,  Shanshan Wang 5,  Ling Qi 6 7
Affiliations

Affiliations

  • 1 Department of Preventive Medicine, Jilin Medical University, Jilin, P.R. China.
  • 2 Department of Emergency and Intensive Medicine, No. 965 Hospital of PLA Joint Logistic Support Force, Jilin, China.
  • 3 Medical Technology College of Beihua University, Jilin, P.R. China.
  • 4 Department of Laboratory Medicine, Jilin Medical University, Jilin, P.R. China.
  • 5 Department of Pathology and Institute of Precision Medicine, Jining Medical University, Jining, China.
  • 6 Department of Pathophysiology, Jilin Medical University, Jilin, China. qiling1718@gzhmu.edu.cn.
  • 7 The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital, Qingyuan, China. qiling1718@gzhmu.edu.cn.
  • # Contributed equally.
PMID: 34453123 DOI: 10.1038/s41417-021-00378-6
Abstract

MicroRNAs (miRNAs or miRs) can be delivered from acute myeloid leukemia (AML) cells to hematopoietic stem cells (HSCs) to regulate hematopoietic function via extracellular vesicles (EVs). In this study, we investigated the roles played by EVs that transport miR-548ac from AML cells in normal hematopoiesis. Bioinformatics analysis demonstrated that miR-548ac was highly expressed in AML-derived EVs. The expression of miR-548ac and TRIM28 and the targeting relationship were identified, and the results demonstrated that the expression of miR-548ac was upregulated in AML cell lines and AML cell-secreted EVs compared with CD34+ HSCs. AML-derived EVs targeted CD34+ HSCs to induce decreased expression of TRIM28 and downstream activation of STAT3. Exosomal miR-548ac was transferred into CD34+ HSCs to target TRIM28. Through gain- and loss-of-function assays, it was observed that the abrogated expression of miR-548ac or STAT3 promoted colony-forming units (CFU), whereas overexpressed miR-548ac repressed CFU, which was rescued by overexpression of TRIM28. Taken together, these results indicated that miR-548ac delivered by AML cell-derived EVs inhibits hematopoiesis via TRIM28-dependent STAT3 activation.

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