RNA-seq analysis of SKMEL28 melanoma cells following DIRC3 and IGFBP5 ASO knockdown
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PROVIDER: PRJNA531445 | ENA |
REPOSITORIES: ENA
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Project description:We identified genes regulated by the DIRC3 long non-coding RNA and its neighbouring tumour suppressor gene IGFBP5 and determined common targets. DIRC3 and IGFBP5 were knocked down by transient transfection of antisense oligonucleotides (ASOs) in the human melanoma cell line Sk-Mel-28. RNA was extracted 72 hours after transfection and polyA selected 150-bp paired end RNA sequencing was performed on the Illumina HiSeq4000 .
2019-11-08 | GSE129467 | GEO
Project description:IGFBP5, a critical regulators of insulin-like growth factors, has been reported to be involved in many kinds of carcinogenesis and cancer metastases. The role of IGFBP5 in human malignant melanoma (MM), however, remains largely unknown. In this study, we demonstrated that IGFBP5 was aberrantly expressed in human melanoma cells and cancer tissues. Overexpression of IGFBP5 dramatically inhibited the proliferation, migration and invasion of human melanoma cells, whereas knockdown of IGFBP5 by shRNA resulted in the opposite effects, enhanced the cell proliferation, migration and metastasis. In addition, IGFBP5 overexpression suppressed the growth and metastasis of melanoma xenograft tumor in vivo and IGFBP5 overexpression inhibited epithelialâmesenchymal transition (EMT) phenotype and stem cell property of tumor cell, with decreased expression of HIF1α, E-cadherin and stem cell markers NANOG, SOX2, OCT4, KLF4 and CD133. Moreover, IGFBP5 exhibited its growth inhibitory activity through inhibition of extracellular signal-regulated Kinase (ERK) and P38-MAPK signaling pathway. Taken together, our findings indicate that IGFBP5 acts as tumor suppressor roles in MM through the modulation of ERK1/2 and P38-MAPK signaling pathway as well as EMT procession and cell stemness, suggesting IGFBP5 as a novel target for human melanoma diagnosis and therapy. mRNA profiles of IGFBP5 over expression (OE) in A375 and A375 cell line were generated using Ion torrent
2016-01-05 | E-GEOD-64693 | biostudies-arrayexpress
Project description:Transcriptome profiling of WM3248 melanoma cells following PGC1-alpha knockdown
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Project description:IGFBP5, a critical regulators of insulin-like growth factors, has been reported to be involved in many kinds of carcinogenesis and cancer metastases. The role of IGFBP5 in human malignant melanoma (MM), however, remains largely unknown. In this study, we demonstrated that IGFBP5 was aberrantly expressed in human melanoma cells and cancer tissues. Overexpression of IGFBP5 dramatically inhibited the proliferation, migration and invasion of human melanoma cells, whereas knockdown of IGFBP5 by shRNA resulted in the opposite effects, enhanced the cell proliferation, migration and metastasis. In addition, IGFBP5 overexpression suppressed the growth and metastasis of melanoma xenograft tumor in vivo and IGFBP5 overexpression inhibited epithelial–mesenchymal transition (EMT) phenotype and stem cell property of tumor cell, with decreased expression of HIF1α, E-cadherin and stem cell markers NANOG, SOX2, OCT4, KLF4 and CD133. Moreover, IGFBP5 exhibited its growth inhibitory activity through inhibition of extracellular signal-regulated Kinase (ERK) and P38-MAPK signaling pathway. Taken together, our findings indicate that IGFBP5 acts as tumor suppressor roles in MM through the modulation of ERK1/2 and P38-MAPK signaling pathway as well as EMT procession and cell stemness, suggesting IGFBP5 as a novel target for human melanoma diagnosis and therapy.
2016-01-05 | GSE64693 | GEO
Project description:We performed RNA-seq on HeLa cells treated with MYCASO-3, a non-targeting ASO (NT-ASO), Lipofectamine alone, and untreated cells
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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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Project description:RNA-seq analysis of HeLa cells following MYC inhibition with ASO
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Project description:Purpose: Detailed exploration of de novo Fatty Acid Synthesis (DNFA) transcription regulation and clinical relevance in melanomas. This study was designed to achieve the following goals: 1) determine the impact of SREBP1 depletion on gene expression in metastatic melanoma cells; 2) determine the specificity of ASO and other reagents inhibiting SREBF1 mRNA. Method: RNA-Seq was performed after culture with control and various SREBF1-depleting agents, including pooled siRNAs and individual ASOs, in HT-144 cells. Results: using STAR, we mapped about 2 X 4 million pair-end sequence reads per sample to the human genome (build GRCh38.94) and identified around 2 million annotated transcripts per sample.
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Project description:Astrocyte-specific ion pump α2-Na+/K+-ATPase plays a critical role in the pathogenesis of amyotrophic lateral sclerosis (ALS). Here, we test the effect of Atp1a2 mRNA-specific antisense oligonucleotides (ASOs) to induce α2-Na+/K+-ATPase knockdown in the widely used ALS animal model, SOD1*G93A mice. Two ASOs led to efficient Atp1a2 knockdown and significantly reduced SOD1 aggregation in vivo. Although Atp1a2 ASO-treated mice displayed no off-target or systemic toxicity, the ASO-treated mice exhibited an accelerated disease onset and shorter lifespan than control mice. Transcriptomics studies reveal downregulation of genes involved in oxidative response, metabolic pathways, trans-synaptic signaling, and upregulation of genes involved in glutamate receptor signaling and complement activation, suggesting a potential role for these molecular pathways in de-coupling SOD1 aggregation from survival in Atp1a2 ASO-treated mice. Together, these results reveal a role for α2-Na+/K+-ATPase in SOD1 aggregation and highlight the critical effect of temporal modulation of genetically validated therapeutic targets in neurodegenerative diseases.
2023-11-30 | GSE196843 | GEO
Project description:We elicited ASO-mediated knockdown of mRNAs in the nervous system by targeting the memory-repressor gene Histone deacetylase 2 (Hdac2) in vitro and in vivo. We observed that an Hdac2-targeted ASO not only triggered a reduction in mRNA levels, but also a direct transcriptional suppression of the Hdac2 gene in neurons in vitro. In further in vivo studies, we observed that a single dose of the Hdac2-targeted ASO delivered by intracerebroventricular injection into the central nervous system (CNS) achieved steady-state diminution of Hdac2 mRNA levels that lasted more than 6 months in vivo. Knockdown of this factor resulted in memory enhancement. ASO administration also caused a prolonged alteration of steady-state levels of a set of known memory-associated mRNAs and triggered secondary changes in the epigenome at sites outside of the primary target gene.
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