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Comparative transcriptomic analysis of 3T3-L1 adipocytes with modulated level of Foxk1 and Foxk2 transcription factor

ABSTRACT: Comparative transcriptomic analysis of 3T3-L1 adipocytes with modulated level of Foxk1 and Foxk2 transcription factor

PROVIDER: PRJNA470676 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7140440.fastq.gz	Fastqsanger.gz
	SRR7140450_1.fastq.gz	Fastqsanger.gz
	SRR7140450_2.fastq.gz	Fastqsanger.gz
	SRR7140441_1.fastq.gz	Fastqsanger.gz
	SRR7140441_2.fastq.gz	Fastqsanger.gz

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Comparative transcriptomic analysis of 3T3-L1 adipocytes with modulated level of Foxk1 and Foxk2 transcription factor

Project description:The goal of this study was to apply Next Generation Sequencing analyses to identify genes and pathways regulated by the Foxk1 and Foxk2 transcription factor in 3T3-L1 adipocytes. We found, that series of enzymes involved in metabolism of lipids and carbohydrates, as well as cell migration, proliferation and adhesion are regulated in response to this transcription factor, thereby providing important insight into biological role of Foxk1 and Foxk2 for cells survival and metabolism.

2018-12-01 | GSE114258 | GEO

FoxK1 and FoxK2 cooperate with ORF45 to promote late lytic replication of Kaposi’s sarcoma-associated herpesvirus

Project description:Lytic replication is essential for persistent infection of Kaposi’s sarcoma-associated herpesvirus (KSHV) and the pathogenesis of related diseases, and many cellular pathways are hijacked by KSHV proteins to initiate and control the lytic replication of this virus. However, the machinery involved in KSHV lytic replication from the early to the late phases remains largely undetermined. We previously revealed that KSHV ORF45 plays important roles in late transcription and translation. In the present study, we reveal that the Forkhead box proteins FoxK1 and FoxK2 are ORF45-binding proteins and are essential for KSHV lytic gene expression and virion production and that depletion of FoxK1 or FoxK2 significantly suppresses the expression of many late viral genes. FoxK1 and FoxK2 directly bind to the promoters of several late viral genes, ORF45 augments the promoter binding and transcriptional activity of FoxK1 and FoxK2, and then FoxK1 or FoxK2 cooperates with ORF45 to promote late viral gene expression. Our findings suggest that ORF45 interacts with FoxK1 and FoxK2 and promotes their occupancy on a cluster of late viral promoters and their subsequent transcriptional activity; consequently FoxK1 and FoxK2 promote late gene expression to facilitate KSHV lytic replication.

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O-GlcNAcylation of FOXK1 orchestrates the E2F pathway

Project description:Gene transcription is a highly regulated process, and deregulation of transcription factors activity underlie numerous pathologies including cancer. FOXK1 and FOXK2 (FOXK1/2) transcription factors have recently emerged as important regulators of cell metabolism, autophagy and cell differentiation. While FOXK1/2 possesses many overlapping functions in normal biology, their specific functions as well as deregulation of their transcriptional activity in cancer is less clear and often contradictory. FOXK1, but less FOXK2, is known to have oncogenic properties as higher expression levels of FOXK1 has been observed in several cancers and is correlated with tumor progression, invasion, and metastasis. However, the molecular mechanism by which FOXK1 exert its oncogenic properties in caner remains unknown. Here we show that elevated expression of FOXK1, but not FOXK2, in normal human fibroblasts promotes transcription of E2F target genes associated with increased proliferation and delayed senescence entry. Fibroblasts overexpressing FOXK1 are also more prone to cellular transformation with minimal oncogenic combinations, suggesting important oncogenic proprieties of FOXK1. Mechanistically, we found that FOXK1, but not FOXK2, is specifically modified by O-GlcNAcylation. FOXK1 O-GlcNAcylation is modulated during the cell cycle and its highest levels coincides with the G1/S phase transition. Moreover, FOXK1 O-GlcNAcylation is increased following cell transformation and loss of this modification leads to decreased FOXK1 ability to promote cellular transformation and tumor growth. Cells overexpressing FOXK1 O-GlcNAcylation-defective mutants have lower E2F1 expression, cell proliferation, and tumour growth. Our results define a distinct role of FOXK1 via O-GlcNAcylation in controlling the cell cycle through the orchestration of the E2F pathway.

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