ArticleCell biology and toxicology2026
ZRANB1 depletion inhibits neuroblastoma progression by destabilizing MYCN through EZH2-mediated deubiquitination.
Article in Cell biology and toxicology, 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
backgroundNeuroblastoma (NB) is a common malignant solid tumor in children, notably aggressive in cases with MYCN amplification. Unraveling the mechanisms behind NB progression is crucial for developing targeted therapies. ZRANB1, a deubiquitinating enzyme, has emerged as a significant player in many cancers, but its specific function in NB still to be fully elucidated.
methodsBioinformatic analyses of transcriptomic datasets (GSE85047 and GSE80149) were performed to identify potential MYCN-dependent pro-survival genes. The biological functions of ZRANB1 in NB cells were assessed by CCK-8, colony formation, migration, invasion, and tumor sphere formation assays. Co-IP, Western blot, CHX chase, and ubiquitination assays were performed to assess the regulatory relationship among ZRANB1, EZH2, and MYCN. Catalytically inactive ZRANB1 mutant and in vitro pull-down assays were performed to validate the requirement of deubiquitinase activity and direct interactions. We evaluated the contribution of the ZRANB1-EZH2-MYCN axis to tumor growth using cell-based assays and mouse xenograft models.
resultsZARNB1 was substantially higher in MYCN-amplified BE(2)M17 cell lines. Functional studies demonstrated that ZRANB1 promoted proliferation, migration, and tumorigenicity. Mechanistically, although ZRANB1 did not directly bind MYCN, it formed a ternary complex with EZH2 and MYCN, thereby stabilizing MYCN via EZH2-mediated regulation. Deubiquitinase activity was required for ZRANB1-mediated MYCN stabilization, and direct ZRANB1-EZH2 interaction was confirmed by in vitro pull-down assays.
conclusionsThis study identifies ZRANB1 as an upstream deubiquitinase that stabilizes EZH2, thereby indirectly maintaining MYCN stability in MYCN-amplified neuroblastoma. These findings establish a ZRANB1-EZH2-MYCN regulatory axis and highlight ZRANB1 as a promising therapeutic target in MYCN-amplified NB.
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