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Transcriptome analysis of SREBF1 silencing and overexpression in thyroid cancer cells

ABSTRACT: Transcriptome analysis of SREBF1 silencing and overexpression in thyroid cancer cells

PROVIDER: PRJNA721465 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14219707_1.fastq.gz	Fastqsanger.gz
	SRR14219707_2.fastq.gz	Fastqsanger.gz
	SRR14219708_1.fastq.gz	Fastqsanger.gz
	SRR14219708_2.fastq.gz	Fastqsanger.gz
	SRR14219709_1.fastq.gz	Fastqsanger.gz

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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

Transcriptome analysis of CHI3L1 silencing in thyroid cancer cells

Project description:Transcriptome analysis of CHI3L1 silencing in thyroid cancer cells

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Effects of CRABP1 overexpression on thyroid cancer cell lines

Project description:Effects of CRABP1 overexpression on thyroid cancer cell lines

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Transcriptome analysis of CHI3L1 silencing in thyroid cancer cells

Project description:CHI3L1 (Chitinase-3-like protein 1), also known as YKL-40, has been associated with inflammation and cancer. Transcription profiling analysis was performed in FTC-133 thyroid cancer cells transfected with control siRNA or siRNAs against CHI3L1.

2020-02-12 | GSE145077 | 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

RNA sequencing analysis of TFCP2L1 overexpression in thyroid cancer cells

Project description:RNA sequencing analysis of TFCP2L1 overexpression in thyroid cancer cells

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RNA sequencing analysis of SLC6A15 overexpression in papillary thyroid cancer cells

Project description:Solute Carrier Family 6 Member 15 (SLC6A15) has been found with dysregulated expression in several kinds of cancers. However, its expression pattern and biological functions in papillary thyroid cancer (PTC) remain unknown. To explore the role of SLC6A15 in PTC, transcription profiling analysis was performed in KTC1 cells with or without SLC6A15 overexpression.

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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

Effect of CRABP2 depletion and overexpression on thyroid cancer cell lines

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RNA sequencing analysis of SLC6A15 overexpression in papillary thyroid cancer cells

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