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Table · dataset · 2026

Data Sheet 1_Conditional myeloid-specific deletion of Ube2n hinders YUMM1.7 melanoma growth.pdf

Listed in figshare and Loughborough Research Repository — shown once because both records carry DOI 10.3389/fonc.2026.1932270.s001

<p>The role of UBE2N in myeloid cell-mediated immune suppression in cancer remains undefined.

Description

Here, we examined the function of UBE2N in myeloid cell-mediated tumor progression using a temporally inducible myeloid-specific knockout model (LysM<sup>CreER</sup>Ube2n<sup>fl/fl</sup>). Temporally induced deletion of Ube2n in myeloid cells (Ube2n<sup>MyeKO</sup>) significantly hindered growth of YUMM1.7 melanoma.

This was accompanied by reduced myeloid cell burden within the tumor microenvironment. We observed altered abundance of PD-1, PD-L1, and SPP1 in the Ube2n<sup>MyeKO</sup> tumor microenvironment at the tissue level. In vitro analysis showed that knock-in expression of a catalytically deficient UBE2N<sup>C87S</sup> mutant in bone marrow-derived macrophages (BMDMs) markedly decreased expression of Spp1.

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We observed decreased SPP1 secretion in Ube2n<sup>MyeKO</sup> BMDM-conditioned media (CM). Treatment with Ube2n<sup>MyeKO</sup> BMDM-CM decreased co-expression of PD-1, TIM-3, and LAG-3 on chronically stimulated T cells. Antibody-mediated neutralization of SPP1 in Ube2n<sup>MyeWT</sup> BMDM-CM decreased PD-1 expression on CD8+ T cells.

Together, these findings suggest a role for myeloid UBE2N in YUMM1.7 progression.</p>

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Inferred from text
Cancer 75% · Oncology and carcinogenesis 71%
Provenance · 2 source records, 30 field assertions
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Loughborough Research Repositoryoai:figshare.com:article/339797838 d agoJSON v1
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