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

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

PROVIDER: PRJNA1028999 | ENA |

REPOSITORIES: ENA

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

Project description:In our study, we found that SQLE was critical to osteosarcoma progression. To identify the mechanism of SQLE in osteosarcoma, we conducted the RNA-seq analysis of SQLE knockdown in osteosarcoma cell line U2OS cells.

2024-12-16 | GSE245562 | GEO

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.

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

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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.

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Temporal chromatin accessibility changes define transcriptional states essential for osteosarcoma metastasis [scATAC-Seq]

Project description:Temporal profiling of chromatin accessibility during metastasis revealed dynamic changes in chromatin accessibility during osteosarcoma lung colonization. We sought to determine whether these changes were due to epigenomic reprogramming, or shifts in subclonal frequency. To do this we performed scATAC-seq on MG63.3-GFP cells grown in vitro.

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Mouse model of Osteosarcoma

Project description:expression analysis from a genetically engineered mouse model of osteosarcoma determine the expression profile of mouse osteosarcoma Keywords: disease state analysis

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Ribosomal protein S3 regulates GLI2-mediated osteosarcoma invasion

Project description:It has been reported that GLI2 promotes proliferation, migration, and invasion of mesenchymal stem cell and osteosarcoma cells. To examine the molecular mechanisms of GLI2-mediated osteosarcoma metastasis, we performed a microarray analysis. The gene encoding ribosomal protein S3 (RPS3) was identified as a target of GLI2. Real-time PCR revealed that RPS3 was upregulated in osteosarcoma cell lines compared with normal osteoblast cells. Knockdown of GLI2 decreased RPS3 expression, whereas forced expression of a constitutively active form of GLI2 upregulated the expression of RPS3. RPS3 knockdown by siRNA decreased the migration and invasion of osteosarcoma cells. Although forced expression of constitutively active GLI2 increased the migration of human mesenchymal stem cells, knockdown of RPS3 reduced the up-regulated migration. In contrast, forced expression of RPS3 increased migration and invasion of osteosarcoma cells. Moreover, reduction of migration by GLI2 knockdown was rescued by forced expression of RPS3. Immunohistochemical analysis showed that RPS3 expression was increased in primary osteosarcoma lesions with lung metastases compared with those without. These findings indicate that GLI2–RPS3 signaling may be a marker of invasive osteosarcoma and a therapeutic target for patients with osteosarcoma.

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