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ABSTRACT: Knockdown of SQLE

PROVIDER: PRJNA737171 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR14800284_1.fastq.gz	Fastqsanger.gz
	SRR14800284_2.fastq.gz	Fastqsanger.gz
	SRR14800285_1.fastq.gz	Fastqsanger.gz
	SRR14800285_2.fastq.gz	Fastqsanger.gz
	SRR14800286_1.fastq.gz	Fastqsanger.gz

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Project description:Knockdown of SQLE

| PRJNA737171 | ENA

Gene expression profiling of RKO cells with or without SQLE knockdown.

Project description:RKO cells (WT or SQLE knockdown) were harvested and mRNA were extracted for high-throughput sequencing.

2024-05-20 | GSE232678 | GEO

p53 transcriptionally regulates SQLE to modulate cholesterol synthesis and tumor growth

Project description:Cholesterol is essential for membrane biogenesis, cell proliferation and differentiation. The role of cholesterol in cancer development and the regulation of cholesterol synthesis are still under active investigation. Here we show that under normal-sterol conditions，p53 directly represses the expression of SQLE, a rate-limiting and the first oxygenation enzyme in cholesterol synthesis，in a SREBP2-independent manner. Through transcriptional downregulation of SQLE, p53 represses cholesterol production in vivo and in vitro, leading to tumor growth suppression. Inhibition of SQLE using small interfering RNA (siRNA) or terbinafine (a SQLE inhibitor) reverses the increased cell proliferation caused by p53 deficiency. Conversely, SQLE overexpression or cholesterol addition promotes cell proliferation, particularly in p53 wild-type cells. More importantly, pharmacological inhibition or shRNA-mediated silencing of SQLE restricts nonalcoholic fatty liver disease (NAFLD) -induced liver tumorigenesis in p53 knockout mice. Therefore, our findings reveal a role for p53 in regulating SQLE and cholesterol biosynthesis, and further demonstrate that downregulation of SQLE is critical for p53-mediated tumor suppression.

2021-07-18 | GSE176112 | GEO

Expression data from human Bladder cancer cell line J82 with control or overexpression of SQLE

Project description:Several reports showed that SQLE was upregulated in some types of cancer, and it is essential for cancer development. Herein, to uncover the role of SQLE in BCa, we performed the RNA-seq to detect the gene expression levels in BCa cell line J82 with overexpression of SQLE.

2024-04-28 | GSE231045 | GEO

Gene expression profiling of RKO cells with or without SQLE knockdown.

Project description:Gene expression profiling of RKO cells with or without SQLE knockdown.

| PRJNA973571 | ENA

Endothelial cell heterogeneity in pathological angiogenesis characterized by metabolic transcriptome diversity

Project description:Endothelial cell (EC) metabolism regulates angiogenesis and is an emerging target for anti-angiogenic therapy in tumor and choroidal neovascularization (CNV). In contrast to tumor ECs (TECs), CNV-ECs cannot be isolated for unbiased metabolic target discovery. Here we used scRNA-sequencing to profile 28,337 choroidal ECs (CECs) from mice to in silico distinguish healthy CECs from CNV-ECs. Trajectory inference suggested that CNV-ECs plastically upregulate genes in central carbon metabolism and collagen biosynthesis during differentiation from quiescent postcapillary venous ECs. CEC-tailored genome scale metabolic modeling predicted essentiality of SQLE and ALDH18A1 for proliferation and collagen production, respectively. Comparative analysis in TECs revealed more outspoken metabolic transcriptome heterogeneity in subtypes and consistent upregulation of SQLE and ALDH18A1 across tumor types. Inhibition of SQLE and ALDH18A1 reduced sprouting angiogenesis in vitro. These findings demonstrate the potential of integrated scRNA-seq analysis to identify angiogenic metabolic targets in disease ECs.

2020-06-25 | E-MTAB-8119 | biostudies-arrayexpress

Inhibition of SQLE or FDFT1 in RBE cells by shRNA, or RBE cells treated with lycorine hydrochloride

Project description:High-throughput sequencing was performed to analyze gene expression profiles of RBE cells after the the inhibition of SQLE or FDFT1 by lentiviruses-mediated shRNA, or RBE cells treated with lycorine hydrochloride.

2023-08-18 | GSE240746 | GEO

Small cell lung cancer cell line panel whole proteome analysis

Project description:We conducted a whole proteome analysis of a panel of human small cell lung cancer cell lines that were either sensitive, moderately sensitive, or insensitive to SQLE inhibition to try and identify proteome signatures of sensititivy

2019-01-09 | PXD011896 | Pride

Effect of depletion of SQLE on gene expression of B16F10 Melanoma cells in vivo

Project description:To investigate the function SQLE in the regulation of tumor immune microenvironment, we established B16F10 cell lines in which target gene has been knocked down by shRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells at same time points.

2023-01-01 | GSE216265 | GEO

Doa10/MARCH6 architecture interconnects E3 ligase activity with lipid-binding transmembrane channel to regulate SQLE

Project description:Transmembrane E3 ligases play crucial roles in homeostasis. Much protein and organelle quality control, and metabolic regulation, are determined by ER-resident MARCH6 E3 ligases, including Doa10 in yeast. Here, we present Doa10/MARCH6 structural analysis by cryo-EM and AlphaFold predictions, and a structure-based mutagenesis campaign. The majority of MARCH6/Doa10 adopts a unique circular structure within the membrane. This channel is established by a lipid-binding scaffold, gated by a flexible helical bundle. The ubiquitylation active site is positioned over the channel by connections between the cytosolic E3 ligase RING domain and the membrane-spanning scaffold and gate. Assaying 95 MARCH6 variants for effects on stability of the well-characterized substrate SQLE, which regulates cholesterol levels, revealed crucial roles of the gated channel and RING domain consistent with AlphaFold-models of substrate-engaged and ubiquitylation complexes. SQLE degradation further depends on connections between the channel and RING domain, and lipid binding sites, revealing how interconnected MARCH6/Doa10 elements could orchestrate metabolic signals, substrate binding, and E3 ligase activity.

2024-01-26 | PXD047499 | Pride

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