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Long noncoding RNA DICER1-AS1 functions in methylation regulation on the multi-drugresistance of osteosarcoma cells via miR-34a-5p and GADD45A (mRNA-seq)

ABSTRACT: Long noncoding RNA DICER1-AS1 functions in methylation regulation on the multi-drugresistance of osteosarcoma cells via miR-34a-5p and GADD45A (mRNA-seq)

PROVIDER: PRJNA658093 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12476701.fastq.gz	Fastqsanger.gz
	SRR12476701_1.fastq.gz	Fastqsanger.gz
	SRR12476701_2.fastq.gz	Fastqsanger.gz
	SRR12476702.fastq.gz	Fastqsanger.gz
	SRR12476702_1.fastq.gz	Fastqsanger.gz

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Long noncoding RNA DICER1-AS1 functions in methylation regulation on the multi-drugresistance of osteosarcoma cells via miR-34a-5p and GADD45A

Project description:Long noncoding RNA DICER1-AS1 functions in methylation regulation on the multi-drugresistance of osteosarcoma cells via miR-34a-5p and GADD45A

| PRJNA658089 | ENA

Long noncoding RNA DICER1-AS1 functions in methylation regulation on the multi-drugresistance of osteosarcoma cells via miR-34a-5p and GADD45A (lncRNA-seq)

Project description:Long noncoding RNA DICER1-AS1 functions in methylation regulation on the multi-drugresistance of osteosarcoma cells via miR-34a-5p and GADD45A (lncRNA-seq)

| PRJNA658094 | ENA

Long Noncoding RNA DICER1-AS1 Functions in Methylation Regulation on the Multi-Drugresistance of Osteosarcoma Cells <i>via</i> miR-34a-5p and GADD45A.

Project description:Osteosarcoma (OS) is a common malignant bone tumor that commonly occurs in children and adolescents. Long noncoding RNAs (lncRNAs) are recognized as a novel class of regulators of gene expression associated with tumorigenesis. However, the effect and mechanism of lncRNAs in OS tumorigenesis and drug resistance have not been characterized. The purpose of the study is to screen potential biomarker and therapeutic target against OS. We compared the lncRNA expression profiles between OS cell lines with different drug resistance levels using RNA-seq analysis and found that lncRNA DICER1-AS1 was significantly differentially expressed in multi-drugresistant OS cells SJSA-1 versus multi-drugsensitive OS cells G-292. Bisulfite Sequencing PCR (BSP) assay was performed to analyze the differential methylation status of the promoter region of DICER1-AS1 in four OS cells. Subsequently, in vitro gain- and loss-of-function experiments demonstrated the roles of DICER1-AS1 and miR-34a-5p in the multi-drugresistance of OS cells. The main findings is that DICER1-AS1 directly binds to miR-34a-5p, and their expression has a negative correlation with each other. The hypermethylation of the promoter region of DICER1-AS1 silenced its expression in the drugresistant cells SJSA-1 and MNNG/HOS. Moreover, we found that growth arrest and DNA damage-inducible alpha (GADD45A) participates in the DICER1-AS1/miR-34a-5p-regulated drug resistance of OS cells, probably via the cell cycle/pRb-E2F pathway. Our results revealed DICER1-AS1/miR-34a-5p-regulated drug resistance of OS cells, a new lncRNA-regulated network in OS tumorigenesis, suggested that DICER1-AS1 can be considered as a potential biomarker and therapeutic target against OS cells.

| S-EPMC8299526 | biostudies-literature

Long noncoding RNA DICER1-AS1 functions in methylation regulation on the multi-drugresistance of osteosarcoma cells via miR-34a-5p and GADD45A

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-08-20 | GSE153788 | GEO

Long noncoding RNA DICER1-AS1 functions in methylation regulation on the multi-drugresistance of osteosarcoma cells via miR-34a-5p and GADD45A (mRNA-seq)

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare NGS-derived retinal transcriptome profiling (RNA-seq) to microarray and quantitative reverse transcription polymerase chain reaction (qRT–PCR) methods and to evaluate protocols for optimal high-throughput data analysis Methods: Total RNA was extracted by Trizol reagent, and DNA was produced by gene specific primers or random primers. Illumina-Hiseq 4000 system was used for RNA sequencing and Illumina-Hiseq 2000 system was used for library sequencing (BGI Technology Company). A single-ended library was prepared according to the Illumina-Truseq RNA sample preparation kit (Illumina) scheme The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) followed by ANOVA (ANOVA) and TopHat followed by Cufflinks. qRT–PCR validation was performed using TaqMan and SYBR Green assays Results: Using an optimized data analysis workflow, demonstrating the high degree of sensitivity of the RNA-seq method. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to retinal function. Data analysis with BWA and TopHat workflows revealed a significant overlap yet provided complementary insights in transcriptome profiling. Conclusions: Our study represents the first detailed generated by RNA-seq technology. The optimized data analysis workflows reported here should provide a framework for comparative investigations of expression profiles. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of complex biologic functions.

2020-08-20 | GSE153787 | GEO

Long noncoding RNA DICER1-AS1 functions in methylation regulation on the multi-drugresistance of osteosarcoma cells via miR-34a-5p and GADD45A (lncRNA-seq)

2020-08-20 | GSE153786 | GEO

Identification of downstream target genes of transcription factor ZEB1, lncRNA FGD5-AS1 and miR-34a-5p in gastric cancer

Project description:As one of the most abundant lncRNAs in cells, the biological function of lncRNA FGD5-AS1 remains largely unclear in cancers, especially in gastric cancer (GC). In addition, the reason for such high levels of FGD5-AS1 in cells remains unknown. In this study, FGD5-AS1 was proved to be a ZEB1-related lncRNA which was overexpressed and predicted poor prognosis in GC. Knockdown of FGD5-AS1 decreased GC proliferation in vitro and in vivo.

2023-02-23 | GSE214471 | GEO

Gene expression profile (GEP) of miR-34a-5p-overexpressing CD34+ HPCs

Project description:Primary Myelofibrosis (PMF) is a myeloproliferative neoplasm characterized by hyperplastic megakaryopoiesis and myelofibrosis. Through a gene expression profile (GEP) study we recently highlighted the upregulationof miR-34a-5p in PMF versus healthy donor (HD) CD34+ hematopoietic progenitor cells (HPCs). To shed some light into the role of miR-34a-5p in PMF pathogenesis, here we unravelled the effects of the overexpression of miR-34a-5p in HPCs forcing its expression in HPCs. We showed that enforced expression of miR-34a-5p blocks proliferation and favours the megakaryocyte and monocyte/macrophage commitment of HPCs. Interestingly, we identified lymphoid enhancer-binding factor 1 (LEF1) and nuclear receptor subfamily 4, group A, member 2 (NR4A2) transcripts as miR-34a-5p-targets downregulated after miR-34a-5p overexpression in HPCs as well as in PMF compared with HD HPCs. Remarkably, the knockdown of NR4A2 in HPCs mimicked the antiproliferative effects of miR-34a-5p overexpression, while the silencing of LEF1 phenocopied the effects of miR-34a-5p overexpression in HPCs lineage choice, by stimulating the megakaryocyte and monocyte/macrophage commitment.

2017-03-08 | GSE89156 | GEO

Hela hsa-miR-34a, b-5p, and c transcriptomes

Project description:Comparative transcriptome analysis of Hela cells transfected with hsa-miR-34a,b-5p or c.

2009-05-13 | GSE15957 | GEO

Understanding downstream signaling pathways regulated by miR-34a-5p in articular cartilage by RNA sequencing using miR-34a knock-out mice

Project description:The goal of this study was to determine the role of miR-34a in regulating chondrocyte transcript profiles. Next Generation Sequencing of total RNA extracted from mouse KO and WT chondrocytes revealed 175 significantly differentially expressed genes (84 up, 91 down) in miR-34a KO chondrocytes compared to WT cells. We are currently validating potential direct targets of miR-34a from our NGS data and performing computational pathway analysis to identify novel pathways regulated by miR-34a.

2021-03-08 | GSE133775 | GEO

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