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P2X1 enhances leukemogenesis through PBX3-BCAT1 pathways.

Xiaoxiao He1, Yilu Xu1, Dan Huang1

  • 1Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.

Leukemia
|November 23, 2022
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The study found that ATP, via the P2X1 channel, drives leukemia-initiating cell (LIC) growth in acute myeloid leukemia (AML). Targeting P2X1 inhibited cancer cell proliferation, offering new therapeutic strategies.

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Area of Science:

  • Hematology
  • Cancer Biology
  • Cellular Metabolism

Background:

  • The regulation of leukemia-initiating cells (LICs) by bone marrow niches is not fully understood.
  • Metabolic factors within the niche may play a crucial role in sustaining leukemogenesis.

Purpose of the Study:

  • To investigate the role of the metabolic niche component ATP and its interaction with the ion channel P2X1 in regulating leukemia-initiating cells (LICs).
  • To explore the potential of targeting the ATP-P2X1 pathway for therapeutic intervention in acute myeloid leukemia (AML).

Main Methods:

  • Utilized a murine acute myeloid leukemia (AML) model with P2X1 deletion to assess LIC function and hematopoiesis.
  • Investigated the effects of P2X1 phosphorylation, knockdown, and antagonist treatment on AML cell proliferation and LIC self-renewal.
  • Analyzed the downstream signaling pathway involving PBX3 and BCAT1.

Main Results:

  • ATP induces ion influx in LICs via P2X1, crucial for LIC self-renewal and maintaining functional LIC numbers in AML.
  • P2X1 deletion significantly reduced LICs without impacting normal hematopoiesis.
  • Specific P2X1 phosphorylation sites (S387, T389) are essential for promoting leukemia development.
  • The ATP-P2X1 pathway upregulates PBX3 to activate BCAT1, sustaining LIC fates.
  • P2X1 knockdown and antagonist treatment inhibited proliferation in human AML cell lines and primary cells.

Conclusions:

  • The metabolic niche factor ATP, acting through P2X1, is a key regulator of LIC activities in AML.
  • Targeting the ATP-P2X1 signaling pathway presents a promising therapeutic strategy for AML and potentially other cancer stem cells.