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TOE1 is a β-catenin interacting protein regulating the proliferation of hematopoietic cells through PAK2 modulation.

Stem cell reports 2026 p. 102894

Park H, Sevim O, Wagstaff M, Goff A, Palmer DA, Kim B, Heesom K, Blair A, Newbury SF, Morgan EL, Towler BP, Chevassut TJ, Morgan RG

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Acute myeloid leukemia (AML) is an aggressive hematological malignancy frequently exhibiting deregulated expression/activity/localization of the Wnt signaling mediator β-catenin.

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APA Park H, Sevim O, et al. (2026). TOE1 is a β-catenin interacting protein regulating the proliferation of hematopoietic cells through PAK2 modulation.. Stem cell reports, 102894. https://doi.org/10.1016/j.stemcr.2026.102894
MLA Park H, et al.. "TOE1 is a β-catenin interacting protein regulating the proliferation of hematopoietic cells through PAK2 modulation.." Stem cell reports, 2026, pp. 102894.
PMID 42030941

Abstract

Acute myeloid leukemia (AML) is an aggressive hematological malignancy frequently exhibiting deregulated expression/activity/localization of the Wnt signaling mediator β-catenin. To derive more effective β-catenin targeting strategies, we previously interrogated its interaction network in myeloid cells and identified several putative novel interacting partners, including Target of EGR1 (TOE1); a deadenylase with unknown function in hematological tissue. This study aimed to define TOE1 function in hematopoietic cells and uncover its molecular targets. TOE1 interacted with β-catenin in both primary and immortalized AML cells, and impacted Wnt signaling output through the modulation of lymphoid enhancer-binding factor-1 (LEF-1). AML samples exhibited deregulated TOE1 expression versus normal hematopoietic stem/progenitor cells (HSPCs), and TOE1 depletion suppressed the proliferation of myeloid leukemia cell lines, and primary human HSPCs, partly through a p21-activated-kinase 2 (PAK2) mediated mechanism. In summary, these data reveal TOE1 as a novel regulator of hematopoietic cell proliferation via the modulation of important growth-regulating pathways.

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