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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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			Action	DRS
	SRR16503471_1.fastq.gz	Fastqsanger.gz
	SRR16503471_2.fastq.gz	Fastqsanger.gz
	SRR16503472_1.fastq.gz	Fastqsanger.gz
	SRR16503472_2.fastq.gz	Fastqsanger.gz
	SRR16503473_1.fastq.gz	Fastqsanger.gz

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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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