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• W2065767079 endingPage "5630" @default.
• W2065767079 startingPage "5620" @default.
• W2065767079 abstract "Abstract Asymmetric cell division (ACD) is a physiologic process during development and tissue homeostasis. ACD produces two unequal daughter cells: one has stem/progenitor cell activity and the other has potential for differentiation. Recent studies showed that misregulation of the balance between self-renewal and differentiation by ACD may lead to tumorigenesis in Drosophila neuroblasts. However, it is still largely unknown whether human cancer stem–like cells exhibit ACD or not. Here, using human neuroblastoma cells as an ACD model, we found that MYCN accumulates at spindle poles by GSK-3β phosphorylation during mitosis. In parallel, the ACD-related ubiquitin ligase Trim32 was recruited to spindle poles by CDK1/cyclin B–mediated phosphorylation. Trim32 interacted with MYCN at spindle poles during mitosis, facilitating proteasomal degradation of MYCN at spindle poles and inducing ACD. Trim32 also suppressed sphere formation of neuroblastoma-initiating cells, suggesting that the mechanisms of ACD produce differentiated neuroblastoma cells that will eventually die. Thus, Trim32 is a positive regulator of ACD that acts against MYCN and should be considered as a tumor-suppressor candidate. Our findings offer novel insights into the mechanisms of ACD and clarify its contributions to human tumorigenesis. Cancer Res; 74(19); 5620–30. ©2014 AACR." @default.
• W2065767079 created "2016-06-24" @default.
• W2065767079 creator A5044874282 @default.
• W2065767079 creator A5087018417 @default.
• W2065767079 date "2014-09-30" @default.
• W2065767079 modified "2023-10-14" @default.
• W2065767079 title "Trim32 Facilitates Degradation of MYCN on Spindle Poles and Induces Asymmetric Cell Division in Human Neuroblastoma Cells" @default.
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• W2065767079 doi "https://doi.org/10.1158/0008-5472.can-14-0169" @default.
• W2065767079 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25100564" @default.
• W2065767079 hasPublicationYear "2014" @default.
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