Overexpression of USF1 in HEK293T cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE17300 | GEO | 2009/09/14
SECONDARY ACCESSION(S): PRJNA119035
REPOSITORIES: GEO
Similar Datasets
Project description:Overexpression of USF1 in HEK293T cells in vitro to ascertain the genes downstream of USF1. Will identify direct targets as well as indirect targets of USF1. Keywords: Overexpression of transcription factor to determine downstream targets. Cloned USF1 from cDNA and transiently transfected into HEK293T cells. Total RNA collected 48 hours after transfection. Empty vector used as control. Expression of USF1 was validated using western blot, and qRT-PCR was used to validate differential expression.
2009-09-14 | E-GEOD-17300 | biostudies-arrayexpress
Project description:Liver cancer, including hepatocellular carcinoma (HCC), is a malignant tumor type with high metastasis and mortality rate in worldwide. Upstream transcription factor 1 (USF1) is a canonical transcription factor (TF) and associated with the pathogenesis of several cancers, while its biological functions and molecular targets in HCC are not clear. In this study, we overexpressed USF1 in Huh7 cells and used whole transcriptome profile sequencing (RNA-seq) and chromatin immunoprecipitation sequencing (ChIP-seq) methods to systematically investigate the downstream targets of USF1. Following polymerase chain reaction (PCR) was used to validate the downstream targets. Based on the results, we found USF1 significantly regulated 350 differentially expressed genes (DEGs). Up DEGs were mainly protein coding genes, and enriched in immune and inflammation response pathways; while down DEGs were mainly lncRNAs, indicating the regulatory feature of USF1. We also detected USF1 directly bound to the promoter region of 2492 genes, which may deeply participate in the viral progression and cell proliferation pathways. By integrating these two datasets, we detected 16 overlapped genes, including down lncRNA-NEAT1 and up TF-ETV5. Down lncRNA-NEAT1 showed reverse expression pattern and prognosis result to USF1 in liver cancer patients, while up TF-ETV5 showed consistent result to USF1. Promoter region motif analysis indicated that ETV5 had more binding motifs and genes than USF1 itself for USF1-regulated DEGs, indicating that USF1 may indirectly modulate gene expression by regulating ETV5 expression in Huh7 cells. Finally, we validated the direct interaction between USF1 and the promoter of ETV5 using ChIP-qPCR. In summary, our results demonstrated that USF1 binds to the promoter region of thousands of genes, and affects large part of DEGs by indirectly manner. The downstream genes, including lncRNA-NEAT1 and TF-ETV5, may also tightly participate in the regulated network by USF1 and have potential functions in the progression of HCC. The USF1 and its downstream targets could be used as potential targets for HCC therapy in future.
2023-09-28 | GSE232262 | GEO
Project description:Liver cancer, including hepatocellular carcinoma (HCC), is a malignant tumor type with high metastasis and mortality rate in worldwide. Upstream transcription factor 1 (USF1) is a canonical transcription factor (TF) and associated with the pathogenesis of several cancers, while its biological functions and molecular targets in HCC are not clear. In this study, we overexpressed USF1 in Huh7 cells and used whole transcriptome profile sequencing (RNA-seq) and chromatin immunoprecipitation sequencing (ChIP-seq) methods to systematically investigate the downstream targets of USF1. Following polymerase chain reaction (PCR) was used to validate the downstream targets. Based on the results, we found USF1 significantly regulated 350 differentially expressed genes (DEGs). Up DEGs were mainly protein coding genes, and enriched in immune and inflammation response pathways; while down DEGs were mainly lncRNAs, indicating the regulatory feature of USF1. We also detected USF1 directly bound to the promoter region of 2492 genes, which may deeply participate in the viral progression and cell proliferation pathways. By integrating these two datasets, we detected 16 overlapped genes, including down lncRNA-NEAT1 and up TF-ETV5. Down lncRNA-NEAT1 showed reverse expression pattern and prognosis result to USF1 in liver cancer patients, while up TF-ETV5 showed consistent result to USF1. Promoter region motif analysis indicated that ETV5 had more binding motifs and genes than USF1 itself for USF1-regulated DEGs, indicating that USF1 may indirectly modulate gene expression by regulating ETV5 expression in Huh7 cells. Finally, we validated the direct interaction between USF1 and the promoter of ETV5 using ChIP-qPCR. In summary, our results demonstrated that USF1 binds to the promoter region of thousands of genes, and affects large part of DEGs by indirectly manner. The downstream genes, including lncRNA-NEAT1 and TF-ETV5, may also tightly participate in the regulated network by USF1 and have potential functions in the progression of HCC. The USF1 and its downstream targets could be used as potential targets for HCC therapy in future.
2023-09-28 | GSE232261 | GEO
Project description:Analysis of adenovirus-mediated USF1 overexpression in liver at gene expression level. Results provide important information of the response of mouse liver to USF1 overexpression, such as specific USF1-induced, suppressed, up- or down-regulated genes invovled in metabolism and immune responses.
2010-03-31 | GSE17442 | GEO
Project description:Analysis of adenovirus-mediated USF1 overexpression in liver at gene expression level. Results provide important information of the response of mouse liver to USF1 overexpression, such as specific USF1-induced, suppressed, up- or down-regulated genes invovled in metabolism and immune responses. Total RNA isolated from whole mouse liver 5 days post tail vein injection of adenovirus carrying either hUSF1 cDNA or eGFP alone as control vector.
2010-04-13 | E-GEOD-17442 | biostudies-arrayexpress
Project description:Macrophage function declines with age, however the underlying mechanisms remain poorly understood. Here, we report that MYC and USF1 are key in driving age-related macrophage functional decline in humans, including reduction in phagocytosis and chemotaxis. We show downregulation with age of MYC and USF1 in human monocyte-derived macrophages (MDMs) and crucially, that knockdown of MYC or USF1 in young MDMs modelled the age-related functional changes. Transcriptomic analysis of these young knockdown MDMs revealed alteration in expression of genes crucial to these functions, as well as those linked to adhesion and extracellular matrix formation. Concordant dysregulation of these genes was also seen in older MDMs. Finally, we show that morphology and F-actin content were altered with loss of MYC or USF1, similarly to that seen in ageing. Together, these results define MYC and USF1 as key drivers of MDM age-related functional decline and identify downstream targets to improve macrophage function in ageing.
2024-04-10 | GSE240075 | GEO
Project description:Translatome analyses of HEK293T upon NSP12 overexpression
| PRJNA757696 | ENA
Project description:Comparison of gene expression for individuals affected with FCHL exhibiting the USF1 susceptibility haplotype and FCHL affected indiviuals carrying the protective haplotype Keywords: ordered
2004-02-29 | GSE590 | GEO
Project description:Transcriptome analyses of HEK293T and VERO upon overexpression
| PRJNA757693 | ENA