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Na+/K+-ATPase Modulates Purinergic P2X3 Receptor Function to Drive Bone Cancer Pain

Published:20 October 2025 DOI: 10.34133/research.0932 PMID: 41122266
Songqiang Huang,?Bo Peng,?Wanting Dong,?Jiapeng He,?Hanbin Chen,?Jin-Song Bian

Abstract

Bone cancer pain (BCP) is one of the most common types of chronic pain in cancer patients, with a prevalence of up to 75%. However, the pathological mechanism and therapeutic approaches are limited. Here, we demonstrated that Na+/K+-ATPase α1 (NKAα1) is a critical regulator of nociception through interaction with purinergic P2X3 receptor (P2X3R) in the dorsal root ganglion (DRG). Conditional knockout of NKAα1 in transient receptor potential vanilloid 1-positive (TRPV1+) neurons led to an increase in P2X3R-dependent Ca2+ influx and neuronal hyperexcitability and also promoted pain hypersensitivity in BCP model mice. In addition, NKAα1 knockout in TRPV1+ neurons further enhanced C-C motif chemokine ligand 5 release, thereby exacerbating spinal glial cell activation and pain hypersensitivity in BCP mice. DR5-12D, a monoclonal antibody to stabilize the expression of NKAα1, markedly inhibited the hyperexcitability of DRG nociceptors and ameliorated pain hypersensitivity in BCP mice. Overall, NKAα1 modulates P2X3R-dependent Ca2+ influx and the excitability of DRG nociceptors, thereby providing valuable theoretical guidance for the treatment of BCP.

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Procduct Name CAS Molecular Formula Supplier Price
Capsaicin 404-86-4 C18H27NO3 858 suppliers $28.00-$3629.00
Capsaicin 404-86-4 C18H27NO3 858 suppliers $28.00-$3629.00
Capsaicin 404-86-4 C18H27NO3 858 suppliers $28.00-$3629.00
Capsaicin 404-86-4 C18H27NO3 858 suppliers $28.00-$3629.00
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