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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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RNA sequencing to determine gene expression changes in SQLE knockdown osteosarcoma cells

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

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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.

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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.

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

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RNA sequencing to determine gene expression changes in SQLE knockdown osteosarcoma cells

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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.

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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.

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