ArticleFrontiers in pediatrics2025
P2RX1 promotes mitochondrial apoptosis via calcium/CaM KII-mediated suppression of PI3K/Akt signaling in Philadelphia chromosome-positive acute lymphoblastic leukemia.
Article in Frontiers in pediatrics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph Methods: By analyzing P2RX1 expression levels in an online patient database and its association with prognosis, we evaluated the potential significance of this receptor in clinical outcomes. A P2RX1 overexpression model was established in the SUP-B15 Ph Results: Analysis of the online patient database revealed that high expression of P2RX1 was significantly associated with poor clinical outcomes. Functional experiments demonstrated that overexpression of P2RX1 in SUP-B15 cells markedly enhanced their sensitivity to apoptosis induced by tyrosine kinase inhibitors; conversely, treatment with the CaMKII inhibitor KN-62 significantly suppressed cell proliferation. Mechanistically, excessive P2RX1 activation disrupts intracellular calcium homeostasis, leading to reduced mitochondrial membrane potential and ATP depletion, thereby activating the intrinsic apoptotic pathway. This process involves inhibition of the PI3K/Akt signaling pathway, hyperactivation of CaMKII, and upregulation of pro-apoptotic proteins such as BAX, Bad, cytochrome C, and cleaved caspase-3 and cleaved caspase-9. Conclusion: This study reveals the role of P2RX1 as a calcium-regulated tumor suppressor in Ph
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