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Gene expression profiling of HCCLM3 cells: Control ASO vs SCARNA13 ASO

ABSTRACT: Gene expression profiling of HCCLM3 cells: Control ASO vs SCARNA13 ASO

PROVIDER: PRJNA491641 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7868083_1.fastq.gz	Fastqsanger.gz
	SRR7868083_2.fastq.gz	Fastqsanger.gz
	SRR7868084_1.fastq.gz	Fastqsanger.gz
	SRR7868084_2.fastq.gz	Fastqsanger.gz
	SRR7868085_1.fastq.gz	Fastqsanger.gz

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Project description:Transcriptional profiling of mouse liver comparing control, scrambled-oligonucleotides (Cont)-treated mice with Perilipin 2-antisense oligonucleotides (Plin2-ASO)-treated mice. C57BL/6 mice on a high-fat diet were treated with oligonucleotides in vivo. The goal was to determine the effects of Plin2 down-regulation in the liver on global gene expression. Two-condition experiment, control oligonucleotides vs. Plin2-antisense oligonucleotides. Biological replicates: 4 control replicates, 4 Plin2-ASO replicates.

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Gene expression profiling of HCCLM3 cells: Control ASO vs SCARNA13 ASO

Project description:Understanding the roles of ncRNAs in tumorigenesis and metastasis would establish avenues for the identification of diagnostic and therapeutic targets. We observed that lncRNA SNHG10 and its derived SCARNA13 were concomitantly upregulated in hepatocellular carcinoma (HCC) pulmonary metastases and associated with poor prognosis. Mechanistically, SCARNA13, modulated by SNHG10, facilitated the cell cycle and epithelial-mesenchymal transition (EMT) of HCC cells by promoting SOX9. SNHG10 served as a sponge for miR-150-5p and interacted with RPL4 mRNA to increase the expression and activity of c-Myb. Reciprocally, upregulated and hyperactivated c-Myb enhanced SNHG10 and SCARNA13 expression through regulating SNHG10 promoter activity, forming a positive feedback loop and continuously stimulating SCARNA13 expression. Our findings characterized a complex epigenetic cause of HCC with clinical implications.

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A Biodistribution Study of OTV vs. ASO by Intravenous or Intrathecal Administration in Cynomolgus Monkeys

Project description:The objective of this study is to evaluate ASO biodistribution and pharmacodynamic response following intravenous delivery of conjugated OTV, which utilizes transferrin-receptor binding to deliver ASO, vs. intrathecal delivery of naked ASO in cynomolgus monkeys, the current gold standard for ASO delivery. Three groups were included for comparison: 1) Negative control cohort = Four biweekly intravenous doses of saline (n=3); 2) IT cohort = Single intrathecal dose of 4mg MALAT1 ASO (n=3); 3)  OTV multi dose cohort = Four biweekly intravenous doses of 30mpk OTV:MALAT1 (n=3). Tissues were collected two weeks after the final dose to allow sufficient time for target knockdown. Brain, spinal cord, and peripheral tissues were dissected and frozen for molecular analysis. Compared to an intrathecal injection of ASO, systemic administration of OTV resulted in significantly more homogenous biodistribution of ASO in the central nervous system as measured by a probe-based hybridization assay as well as staining with an anti-ASO antibody. One potential consequence of heterogeneous ASO distribution is heterogeneous target knockdown throughout the CNS. We observed more consistent target knockdown throughout the cortex, subcortical areas, and spinal cord of monkeys dosed peripherally with OTV. By contrast, monkeys dosed intrathecally with naked ASO showed much more knockdown in the spinal cord compared to the brian, consistent with ASO distribution.

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