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RNA-seq approach to study the specific effects of SREBF1-depleting antisense oligonucleotide (ASO) reagent in human melanoma cells.

ABSTRACT: Purpose: Detailed exploration of de novo Fatty Acid Synthesis (DNFA) transcription regulation and clinical relevance in melanomas. This study was designed to achieve the following goals: 1) determine the impact of SREBP1 depletion on gene expression in metastatic melanoma cells; 2) determine the specificity of ASO and other reagents inhibiting SREBF1 mRNA. Method: RNA-Seq was performed after culture with control and various SREBF1-depleting agents, including pooled siRNAs and individual ASOs, in HT-144 cells. Results: using STAR, we mapped about 2 X 4 million pair-end sequence reads per sample to the human genome (build GRCh38.94) and identified around 2 million annotated transcripts per sample.

ORGANISM(S): Homo sapiens

PROVIDER: GSE122707 | GEO | 2018/11/20

REPOSITORIES: GEO

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RNA-seq approach to study the specific effects of SREBF1-depleting antisense oligonucleotide (ASO) reagent in human melanoma cells.

Project description:RNA-seq approach to study the specific effects of SREBF1-depleting antisense oligonucleotide (ASO) reagent in human melanoma cells.

| PRJNA506045 | ENA

Next Generation Sequencing Facilitates Quantitative Analysis of Bone Marrow-Derived Macrophages Transcriptomes for Acly-E14 ASO effects

Project description:Purpose: The purpose of this study is to detect activated or silenced genes during bone marrow derived macrophages (BMDMs) transfected with control siRNA or Acly-E14 siRNA. Gene expression differences between two samples could be found using transcriptome profiling (RNA-seq) analysis. Methods: Mouse BMDMs were generated from bone marrow cells in RPMI-1640 medium with recombinant mouse M-CSF (20ng/ml). BMDMs were stained to confirm the surface expression of CD11b and F4/80. Cells with purity >97.5% were used for subsequent experiments. BMDMs were transfected with control ASO or Acly-E14 ASO. 48 hour later, they were stimulated with LPS (100ng/ml) for 4 hours, of which RNA profiles were generated by deep sequencing, using Illumina. Results: We mapped about 10 million sequence reads per sample to the mouse genome, identified hundreds of genes with significant mRNA variation between BMDMs transfected with the indicated ASOs.

2024-11-06 | GSE272304 | GEO

CREB regulated transcriptional coactivator 2 proteome landscape is plausibly modulated by SREBF1

Project description:CRTC2 is a critical transcription cofactor that induces the glucose homeostatic genes by activating CREB. However, energy homeostasis is maintained by multiple pathways, therefore, it is possible that CRTC2 may interact with other transcription factors, especially under metabolic stress. Thereby, CRTC2 liver-specific knockout mice were created and the global proteome, phosphoproteome and acetylome from liver tissue under the high fat diet conditions were analyzed using liquid chromatography-tandem mass spectrometry (LC-MS/MS) and bioinformatics analysis. As expected, differentially expressed proteins (DEPs) are enriched in metabolic pathways that were subsequently corroborated by animal experiments. The consensus DEPs from these datasets were used as seed proteins to generate a protein-protein interaction (PPI) network using STRING and GeneMANIA identified fatty acid synthase (FASN) as the mutually relevant protein. Additional local-PPI (LPPI) analysis of CRTC2 and FASN with DEPs, SREBF1 was found to be a common mediator. CRTC2/CREB and SREBF1 are transcription factors, DNA-binding motif analysis showed multiple CRTC2/CREB regulated genes also possess SREBF1 binding motifs that unveil the possible induction by CRTC2/SREBF1 complex, which is reinforced by structural analysis. Thus, CRTC2/SREBF1 complex plausibly modulate the transcription of multiple proteins that fine-tune the cellular metabolism under metabolic stress.

2023-10-24 | PXD039817 | Pride

Srebf1-mediated fatty acid metabolism is crucial to sustain sugmented pigmentation SREBF1-mediated metabolic reprogramming through fatty acid metabolism sustains augmented melanogenesis

Project description:Methods: mRNA profiles of B16 mouse melanoma cell line during pigmentation induced by culturing at low density were generated by deep sequencing, in dublicate. Library preparation was done using trueseq 4000 for quencing on Illumina paired end sequencing. The sequence read that passed the quality filter were aligned with GRCm38 as reference genome. Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample and identified 18753 transcripts in the pigmenting B16 melanocytes from D3 to D7 using HTSeq tool. R-values from Corelation plot varies from 0.98-0.99 between two replicates for different days.

2022-04-19 | GSE164375 | GEO

Caspase-4 mediates SREBP1 activation in macrophages

Project description:We identified caspase-4/S1P/SREBP1 pathway that is activated in LPS-treated macrophages. To analyze the functions of caspase-4 and SREBP1 in gene expression in macrophages, we analyzed the effects of deletions of Casp4 and Srebf1 in bone marrow-derived macrophages by RNA-seq.

2023-01-09 | GSE208374 | GEO

RNA-seq in SREBF1-deficient human iPSCs, hiPSC-NSCs and differentiated cells.

Project description:Omics analyses and qRT-PCR time-course during the transition from hiPSC to hiPSC-NSC highlighted the up-regulation of SREBF1, a gene involved in cholesterol biosynthesis and lipid homeostasis, suggesting its potential role in NSC commitment/maintenance. To test this hypothesis, we generated SREBF1-deficient hiPSC lines by co-delivering ribonucleoprotein Cas9 with a pool of sgRNA targeting exon 5 of the SREBF1 gene. Upon isolation of three clones harboring the deletion we performed RNA-seq analysis in hiPSC, hiPSC-NSC and differentiated cultures at 7 and 14 days of differentiation, compared to control cells. This analysis will allow to identify the potential role of SREBF1 in affecting hiPSC-to-hiPSC-NSC transition, hiPSC-NSC maintenance and commitment toward differentiated cell populations.

2024-09-23 | GSE273125 | GEO

Transcriptome analysis of SREBF1 silencing and overexpression in thyroid cancer cells

Project description:Malignant thyroid tumors have altered lipid metabolism. Sterol regulatory element-binding transcription factor 1 (SREBF1), also known as sterol regulatory element-binding protein 1 (SREBP-1), regulates cellular lipid homeostasis. We found that SREBF1 expression is a prognostic factor in patients with thyroid cancer and planned to elucidate its oncogenic mechanisms.

2021-04-13 | GSE171966 | GEO

ARMC5 selectively degrades SCAP-free SREBF1 and is essential for fatty acid desaturation in adipocytes

Project description:Background: Armadillo repeat containing 5 (ARMC5)-CUL3 complex was recently identified as an E3 ubiquitin ligase of full-length SREBF. Although ARMC5 was involved in SREBF2 pathway in the adrenocortical cells and might participate in the development of primary bilateral macronodular adrenal hyperplasia (PBMAH), the role of ARMC5 in adipocytes has not been investigated. Methods and Results: Adipocyte-specific Armc5 knockout mice were generated. In the white adipose tissue (WAT) of these mice, all the stearoyl-CoA desaturase (Scd) were drastically downregulated under refed condition and high fat-high sucrose diet. Consistently, unsaturated fatty acids were decreased, while saturated fatty acids were increased in the WAT of these mice. Assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-Seq) peaks at the SREBF1-binding sites were markedly diminished around the Scd1 locus in the WAT of adipocyte-specific Armc5 knockout mice. Armc5-deficient 3T3-L1 adipocytes also exhibited downregulation of Scd. Mechanistically, disruption of Armc5 restored decreased full-length SREBF1 in the CHO cells deficient for Scap, an escort protein required for the transport of SREBF from the ER to the Golgi. In HEK293T cells, overexpression of Scap inhibited ARMC5-mediated degradation of full-length SREBF1, and overexpression of Armc5 increased nuclear SREBF1/full-length SREBF1 ratio in the presence of exogenous Scap in HEK293T cells. Conclusions: ARMC5 exerts selective removal of SCAP-free SREBF1 and stimulates SCAP-mediated SREBF1 processing, hence is essential for fatty acid desaturation in vivo.

2024-12-19 | GSE262941 | GEO

ARMC5 selectively degrades SCAP-free SREBF1 and is essential for fatty acid desaturation in adipocytes.

2025-04-08 | GSE264274 | GEO

Role of SREBP1 in macrophages during muscle regeneration

Project description:The purpose of this study is to investigate how SREBP1a in macrophages regulates cellular function during muscle regeneration process after injury. We report that the systemic deletion of Srebf1, encoding SREBP1, and macrophage-specific deletion of Srebf1a, encoding SREBP1a, delays the resolution of inflammation, and impairs skeletal muscle regeneration after injury. Srebf1 deficiency impairs mitochondrial function of macrophages and suppresses the accumulation of reparative macrophages to the injured site.

2023-12-17 | GSE232394 | GEO

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