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SAPCD2 promotes neuroblastoma progression by altering the subcellular distribution of E2F7

ABSTRACT: SAPCD2 promotes neuroblastoma progression by altering the subcellular distribution of E2F7

PROVIDER: PRJNA773069 | ENA |

REPOSITORIES: ENA

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SAPCD2 promotes neuroblastoma progression by altering the subcellular distribution of E2F7

Project description:We report a previously unrecognized role of SAPCD2 in E2F signaling pathway in neuroblastoma. To explore SAPCD2-dependent gene regulation, RNA-seq analysis was conducted and the differently expressed genes were revealed in the SAPCD2-knockdown SK-N-BE(2) cells in comparison to control group. We find that SAPCD2 contributes to E2F7 mislocalization and decreases the level of nuclear E2F7 in NB cells, thus restraining the inhibitory effect of nuclear E2F7 on E2F signaling pathway. SAPCD2 knockdown limits the overactivation of E2F signaling in NB cells, affects the expression of genes involved in cell cycle and chromosome stability, and thereby blocking tumor progression.

2022-01-23 | GSE186245 | GEO

SAPCD2 promotes neuroblastoma progression by altering the subcellular distribution of E2F7.

Project description:Recent studies uncovered the emerging roles of SAPCD2 (suppressor anaphase-promoting complex domain containing 2) in several types of human cancer. However, the functions and underlying mechanisms of SAPCD2 in the progression of neuroblastoma (NB) remain elusive. Herein, through integrative analysis of public datasets and regulatory network of GSK-J4, a small-molecule drug with anti-NB activity, we identified SAPCD2 as an appealing target with a high connection to poor prognosis in NB. SAPCD2 promoted NB progression in vitro and in vivo. Mechanistically, SAPCD2 could directly bind to cytoplasmic E2F7 but not E2F1, alter the subcellular distribution of E2F7 and regulate E2F activity. Among the E2F family members, the roles of E2F7 in NB are poorly understood. We found that an increasing level of nuclear E2F7 was induced by SAPCD2 knockdown, thereby affecting the expression of genes involved in the cell cycle and chromosome instability. In addition, Selinexor (KTP-330), a clinically available inhibitor of exportin 1 (XPO1), could induce nuclear accumulation of E2F7 and suppress the growth of NB. Overall, our studies suggested a previously unrecognized role of SAPCD2 in the E2F signaling pathway and a potential therapeutic approach for NB, as well as clues for understanding the differences in subcellular distribution of E2F1 and E2F7 during their nucleocytoplasmic shuttling.

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Subcellular distribution of RNAs in HeLa cells

Project description:HeLa cells were fractioned in nucleus and cytoplasm to investigate the subcellular distribution of lncRNAs.

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E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells

Project description:This SuperSeries is composed of the following subset Series: GSE32353: Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells (nCounter) GSE32354: Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null liver (Affymetrix) Refer to individual Series

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Genome wide maps of E2F7 binding in IMR90 cells

Project description:Oncogene-induced senescence is an anti-proliferative stress response program that acts as a fail-safe mechanism to limit oncogenic transformation and is regulated by the retinoblastoma protein (RB) and p53 tumor suppressor pathways. We identify the atypical E2F family member E2F7 as the only E2F transcription factor potently upregulated during oncogene-induced senescence, a setting where it acts in response to p53 as a direct transcriptional target. Once induced, E2F7 binds and represses a series of E2F target genes and cooperates with RB to efficiently promote cell cycle arrest and limit oncogenic transformation. Disruption of RB triggers a further increase in E2F7, which induces a second cell cycle checkpoint that prevents unconstrained cell division despite aberrant DNA replication. Mechanistically, E2F7 compensates for the loss of RB in repressing mitotic E2F target genes.

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