ArticleThe FEBS journal2026
The interaction between NPMc+ and Orai1 induces abnormal calcium influx to facilitate leukemogenesis.
Article in The FEBS journal, 2026. 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
Nucleophosmin 1 (NPM1) is a ubiquitously expressed phosphoprotein, mainly located in the nucleolus. It is overexpressed in solid tumors and considered a key target in cancer therapy. NPM1 mutations are the most common genetic abnormalities in acute myeloid leukemia (AML), where they are found in about 30% of patients. In AML, NPM1 mutations result in the cytoplasmic localization of the mutant protein NPMc+. Although NPM1 mutations are known to drive AML, the underlying mechanisms are not fully understood. In this study, we found that primary leukemia cells from NPM1-mutated AML patients exhibited elevated intracellular calcium levels compared with cells from NPM1 wild-type AML patients. Our investigation revealed that NPMc+ interacts with the calcium channel Orai1, disrupting calcium homeostasis in AML cells. Notably, we identified that the N-terminal region of NPM1 contains a calcium-binding domain that directly interacts with Orai1, facilitating calcium influx. Targeting NPMc+, Orai1, or the NPMc+/Orai1 complex using small-molecule inhibitors significantly reduced calcium influx, inhibited calcium-related signaling pathways, and suppressed the proliferation of NPM1-mutated AML cells. These findings uncover a novel mechanism in which NPMc+ interacts with Orai1, disrupting calcium homeostasis and promoting AML progression. This presents a promising therapeutic strategy targeting the NPMc+/Orai1-mediated calcium imbalance in NPM1-mutated AML.
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