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BBX regulates corticogenesis by repressing p53-mediated p21 expression. [set 2]

ABSTRACT: This study aims to elucidate the role of BBX in embryonic neural stem cell maintenance. For mechanism study, we used mRNA sequencing to profile the transcriptional expression of E13.5 NSC upon BBX knockdown and BBX+p21 co-knockdown.

ORGANISM(S): Mus musculus

PROVIDER: GSE337091 | GEO | 2026/07/17

REPOSITORIES: GEO

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BBX regulates corticogenesis by repressing p53-mediated p21 expression.

Project description:This study aims to elucidate the role of BBX in embryonic neural stem cell maintenance. For mechanism study, we used mRNA sequencing to profile the transcriptional expression of E13.5 NSC upon BBX knockdown.

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Rack1 is Essential for Corticogenesis by Preventing P21-Dependent Senescence in Neural Stem Cells

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Project description:The cyclin-dependent kinase inhibitor p21WAF1/Cip1 (p21) is a cell-cycle checkpoint effector and inducer of senescence, regulated by p53. Yet, evidence suggests that, through a so-far obscure mechanism, p21 could also be oncogenic. We report that a subset of atypical cancerous cells strongly expressing p21 showed proliferation features. This occurred predominantly in p53-mutant human cancers suggesting p53-independent upregulation of p21 selectively in more aggressive tumour cells. Multifaceted phenotypic and genomic analyses of p21-inducible, p53-null, cancerous and near-normal cellular models showed that after an initial senescence-like phase, a subpopulation of p21-expressing proliferating cells emerged, featuring increased genomic instability, aggressiveness and chemo-resistance. Mechanistically, sustained p21-accumulation inhibited mainly the CRL4CDT2 ubiquitin-ligase, leading to deregulated origin licensing and replication stress. Collectively, our data reveal tumour-promoting ability of p21 through deregulation of DNA replication licensing machinery, an unorthodox role to be considered in cancer treatment, since p21 responds to various stimuli including some chemotherapy drugs.

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