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SREBF1 coordinates with master transcription factors in regulating lipid metabolism and cancer-promoting pathways in squamous cell carcinoma

ABSTRACT: SREBF1 coordinates with master transcription factors in regulating lipid metabolism and cancer-promoting pathways in squamous cell carcinoma

PROVIDER: PRJNA601742 | ENA |

REPOSITORIES: ENA

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SREBF1 coordinates with master transcription factors in regulating lipid metabolism and cancer-promoting pathways in squamous cell carcinoma

Project description:We profiled esophageal squamous cell carcinorma (ESCC) cell lines with chromatin immunoprecipitation sequencing (ChIP-Seq). Mathematically modeling was performed to establish (super)-enhancers landscapes and inter-connected transcriptional circuitry formed by master TFs. Coregulation and cooperation between master TFs was investigated by ChIP-Seq, RNASeq, 4C-Seq and luciferase assay. Biological functions of candidate factors were evaluated by measuring cell proliferation, colony formation, cell apoptosis and xenograft growth. Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. Here, we aim to compare of ESCC cells knock down SREBF1 with siRNA and negative control transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis. We also report the application of circular chromatin conformation capture (4C) sequencing technology for studying master transcription factor (SREBF1) in human ESCC cancer cell lines (TE5).

2020-06-15 | GSE143803 | GEO

SREBF1 coordinates with master transcription factors in regulating lipid metabolism and cancer-promoting pathways in squamous cell carcinoma [4C]

Project description:SREBF1 coordinates with master transcription factors in regulating lipid metabolism and cancer-promoting pathways in squamous cell carcinoma [4C]

| PRJNA741506 | ENA

SREBF1 coordinates with master transcription factors in regulating lipid metabolism and cancer-promoting pathways in squamous cell carcinoma [4C]

Project description:To determine whether a TP63/KLF5-regulated super-enhancer region can impact SREBF1 transcription, circularized chromosome conformation capture (4C) assays were performed. 4C assays identified complex, extensive interactions between the SREBF1 promoter and the super-enhancer region Moreover, these DNA-DNA contacts were strictly confined within the super-enhancer region, highlighting the specificity of chromatin interactions

2021-06-26 | GSE178923 | GEO

Interplay and cooperation between SREBF1 and master transcription factors regulate lipid metabolism and tumor-promoting pathways in squamous cancer.

Project description: Not available

| S-EPMC8285542 | biostudies-literature

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

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

Transcriptomic analysis of active form of Srebf1-overexpressed fibroblasts in bleomycin-induced lung fibrosis

Project description:Pulmonary fibrosis (PF) is an intractable disorder with a poor prognosis. Although lung fibroblasts play central roles in PF, their key regulatory molecules remain unclear. We performed transcriptome analysis of lung fibroblasts from bleomycin- and silica-treated murine lungs and identified 55 hub transcription factors highly connected to gene modules differentially expressed in PF. To elucidate whether fibroblast-specific intervention against the hub transcription factor Srebf1 modulates pathogenic activation of lung fibroblasts in vivo, we intratracheally-transferred active form of Srebf1-overexpressed fibroblasts into bleomycin-treated lungs and performed global transcriptome analysis.

2019-01-30 | GSE110533 | GEO

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

Project description: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.

2018-11-20 | GSE122707 | GEO

Activation of bivalent factor DLX5 cooperates with master regulator TP63 to promote squamous cell carcinoma [RNA-Seq]

Project description:To reconstruct systematically master regulator transcription factor (MRTF)-dependent transcription networks in squamous cell carcinomas (SCCs), a novel computational method (ELMER) was applied to 1,293 pan-SCC patient samples and identified 44 hyperactive SCC MRTFs. As the top candidate, DLX5 exhibits a notable bifurcate re-configuration of its bivalent promoter in cancer. Specifically, DLX5 maintains a bivalent state in normal tissues; it undergoes de novo DNA hypermethylation and transcriptional repression in multiple non-SCC cancers. In stark contrast, DLX5 promoter gains active histone marks and becomes transcriptionally activated in SCCs, which is mediated directly by SOX2. Functionally, DLX5 is essential for SCC viability, migration, anchorage-independent growth and xenograft proliferation. Mechanistically, DLX5 interacts and cooperates with TP63 to regulate ~2,000 enhancers and promoters, which converge on activating cancer-promoting pathways. Together, our data establish a novel and strong SCC-promoting factor, and elucidate a new epigenomic mechanism - bifurcate chromatin re-configuration - during cancer development.

2021-09-14 | GSE142862 | GEO

Activation of bivalent factor DLX5 cooperates with master regulator TP63 to promote squamous cell carcinoma [ChIP-Seq]

2021-09-14 | GSE142861 | GEO

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