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Table · dataset · 2026

Table 5_USP26-mediated stabilization of RAD51 promotes endometrial cancer progression and limits ferroptosis.xlsx

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Background<p>Ferroptosis is increasingly implicated in endometrial cancer, but the role of the homologous recombination protein RAD51 in ferroptotic stress and its post-translational regulation remain unclear.</p>Methods<p>RAD51 expression was assessed in GEO datasets, UCEC tissues, and endometrial cancer cell lines.

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RAD51 loss-of-function was evaluated using proliferation, cell-death, Transwell, ferroptosis-related, and xenograft assays.

IP–MS, co-immunoprecipitation, cycloheximide chase, proteasome inhibition, ubiquitination assays, USP26-C304S, and RAD51 rescue experiments were used to define USP26-dependent RAD51 regulation.</p>Results<p>RAD51 was upregulated in endometrial cancer and its depletion reduced proliferation and xenograft growth, lowered Transwell migration/invasion readouts, and increased ferroptosis-associated changes. USP26 associated with RAD51, reduced its ubiquitination, and stabilized RAD51 in a catalytic activity-dependent manner.

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RAD51 re-expression partially rescued the effects of USP26 depletion.</p>Conclusions<p>The USP26–RAD51 axis supports endometrial cancer progression and limits ferroptosis-associated stress, identifying RAD51 protein stability as a potential mechanistic vulnerability.</p>

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Cancer 75% · Oncology and carcinogenesis 70% · Tabular 65%
Provenance · 1 source records, 19 field assertions
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