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Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg) II

ABSTRACT: Purpose: Next-generation sequencing (NGS) has used to detect alterations in cellular pathways by various drugs. The goal of this study is to identify alteration of gene expression in human osteochondromas in response to identify nontreated or RARg agonist-treated osteochondorma transcriptome profiling (RNA-seq) and to evaluate the actions of RARg agonists on osteochondromas. Methods: Osteochondroma mRNA profiles of untreated or RARg agonist treated (4 days) osteochondroma explants were generated by deep sequencing, in triplicate, using Illumina HiSeq 4000. 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. Results and Conclusions: Our study represents the detailed analysis of human osteochondromas, with biologic replicates, generated by RNA-seq technology. We conclude that RNA-seq based transcriptome revealed that RARg agonists acts on human osteochondromas and altered various types of biological functions.

ORGANISM(S): Homo sapiens

PROVIDER: GSE181129 | GEO | 2021/07/30

REPOSITORIES: GEO

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Similar Datasets

Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg) I

Project description:Purpose: Next-generation sequencing (NGS) has used to detect alterations in cellular pathways by various drugs. The goal of this study is to identify alteration of gene expression in human osteochondromas in response to identify nontreated or RARg agonist-treated osteochondorma transcriptome profiling (RNA-seq) and to evaluate the actions of RARg agonists on osteochondromas. Methods: Osteochondroma mRNA profiles of untreated or RARg agonist treated (4 days) osteochondroma explants were generated by deep sequencing, in triplicate, using Illumina HiSeq 4000. 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. Results and Conclusions: Our study represents the detailed analysis of human osteochondromas, with biologic replicates, generated by RNA-seq technology. We conclude that RNA-seq based transcriptome revealed that RARg agonists acts on human osteochondromas and altered various types of biological functions.

2021-07-26 | GSE180764 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg)

Project description:Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg)

| PRJNA750773 | ENA

Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg) I

| PRJNA749453 | ENA

Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg) II

| PRJNA750772 | ENA

Next Generation Sequencing Facilitates Quantitative Analysis of Transcriptomes of Osteochondroma Explants Nontreated or Treated with Selective Agonist of Retionic acid Nuclear Receptor Gamma (RARg)

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

2021-07-30 | GSE181133 | GEO

The miR-96 and RARG signaling axis governs androgen signaling and prostate cancer progression VI

Project description:Expression levels of retinoic acid receptor gamma (NR1B3/RARG, encodes RARG), are commonly reduced in prostate cancer (PCa). Therefore we sought to establish the cellular and gene regulatory consequences of reduced RARG expression, and determine RARG regulatory mechanisms. RARG shRNA approaches in non-malignant (RWPE-1 and HPr1-AR) and malignant (LNCaP) prostate models revealed that reducing RARG levels, rather than adding exogenous retinoid ligand, had the greatest impact on prostate cell viability and gene expression. ChIP-Seq defined the RARG cistrome which was significantly enriched at active enhancers associated with AR binding sites. Reflecting a significant genomic role for RARG to regulate androgen signaling, RARG knockdown in HPr1-AR cells significantly regulated the magnitude of the AR transcriptome. RARG down-regulation was explained by increased miR-96 in PCa cell and mouse models, and TCGA PCa cohorts. Biochemical approaches confirmed that miR-96 directly regulated RARG expression and function. Capture of the miR-96 targetome by biotin-miR96 identified that RARG and a number of RARG interacting co-factors including TACC1 were all targeted by miR-96, and expression of these genes were prominently altered, positively and negatively, in the TCGA-PRAD cohort. Differential gene expression analyses between tumors in the TCGA-PRAD cohort with lower quartile expression levels of RARG and TACC1 and upper quartile miR-96, compared to the reverse, identified a gene network including several RARG target genes (e.g. SOX15) that significantly associated with worse disease free survival (hazard ratio 2.23, 95% CI 1.58 to 2.88, p=0.015). In summary, miR-96 targets a RARG network to govern AR signaling, PCa progression and disease outcome. ChIP-seq: RWPE-1-BAC-RARG-EGFP non-malignant, immortalized cell line infected with BAC-RARG-EGFP, +/- 10nM CD437 for 2 hours

2018-07-20 | GSE117179 | GEO

The miR-96 and RARG signaling axis governs androgen signaling and prostate cancer progression V

Project description:Expression levels of retinoic acid receptor gamma (NR1B3/RARG, encodes RARG), are commonly reduced in prostate cancer (PCa). Therefore we sought to establish the cellular and gene regulatory consequences of reduced RARG expression, and determine RARG regulatory mechanisms. RARG shRNA approaches in non-malignant (RWPE-1 and HPr1-AR) and malignant (LNCaP) prostate models revealed that reducing RARG levels, rather than adding exogenous retinoid ligand, had the greatest impact on prostate cell viability and gene expression. ChIP-Seq defined the RARG cistrome which was significantly enriched at active enhancers associated with AR binding sites. Reflecting a significant genomic role for RARG to regulate androgen signaling, RARG knockdown in HPr1-AR cells significantly regulated the magnitude of the AR transcriptome. RARG down-regulation was explained by increased miR-96 in PCa cell and mouse models, and TCGA PCa cohorts. Biochemical approaches confirmed that miR-96 directly regulated RARG expression and function. Capture of the miR-96 targetome by biotin-miR96 identified that RARG and a number of RARG interacting co-factors including TACC1 were all targeted by miR-96, and expression of these genes were prominently altered, positively and negatively, in the TCGA-PRAD cohort. Differential gene expression analyses between tumors in the TCGA-PRAD cohort with lower quartile expression levels of RARG and TACC1 and upper quartile miR-96, compared to the reverse, identified a gene network including several RARG target genes (e.g. SOX15) that significantly associated with worse disease free survival (hazard ratio 2.23, 95% CI 1.58 to 2.88, p=0.015). In summary, miR-96 targets a RARG network to govern AR signaling, PCa progression and disease outcome. RNA-seq: HPr1-AR non-malignant, immortalized cell line +/- shRARG, +/- 10nM DHT for 0,24,96 hours

2018-07-20 | GSE117110 | GEO

The miR-96 and RARG signaling axis governs androgen signaling and prostate cancer progression IV

Project description:Expression levels of retinoic acid receptor gamma (NR1B3/RARG, encodes RARG), are commonly reduced in prostate cancer (PCa). Therefore we sought to establish the cellular and gene regulatory consequences of reduced RARG expression, and determine RARG regulatory mechanisms. RARG shRNA approaches in non-malignant (RWPE-1 and HPr1-AR) and malignant (LNCaP) prostate models revealed that reducing RARG levels, rather than adding exogenous retinoid ligand, had the greatest impact on prostate cell viability and gene expression. ChIP-Seq defined the RARG cistrome which was significantly enriched at active enhancers associated with AR binding sites. Reflecting a significant genomic role for RARG to regulate androgen signaling, RARG knockdown in HPr1-AR cells significantly regulated the magnitude of the AR transcriptome. RARG down-regulation was explained by increased miR-96 in PCa cell and mouse models, and TCGA PCa cohorts. Biochemical approaches confirmed that miR-96 directly regulated RARG expression and function. Capture of the miR-96 targetome by biotin-miR96 identified that RARG and a number of RARG interacting co-factors including TACC1 were all targeted by miR-96, and expression of these genes were prominently altered, positively and negatively, in the TCGA-PRAD cohort. Differential gene expression analyses between tumors in the TCGA-PRAD cohort with lower quartile expression levels of RARG and TACC1 and upper quartile miR-96, compared to the reverse, identified a gene network including several RARG target genes (e.g. SOX15) that significantly associated with worse disease free survival (hazard ratio 2.23, 95% CI 1.58 to 2.88, p=0.015). In summary, miR-96 targets a RARG network to govern AR signaling, PCa progression and disease outcome. RWPE1 non-malignant, immortalized cell line +/- shRARG, +/- 10nM CD437 for 24 hours

2018-07-20 | GSE117104 | GEO

The miR-96 and RARG signaling axis governs androgen signaling and prostate cancer progression III

Project description:Expression levels of retinoic acid receptor gamma (NR1B3/RARG, encodes RARG), are commonly reduced in prostate cancer (PCa). Therefore we sought to establish the cellular and gene regulatory consequences of reduced RARG expression, and determine RARG regulatory mechanisms. RARG shRNA approaches in non-malignant (RWPE-1 and HPr1-AR) and malignant (LNCaP) prostate models revealed that reducing RARG levels, rather than adding exogenous retinoid ligand, had the greatest impact on prostate cell viability and gene expression. ChIP-Seq defined the RARG cistrome which was significantly enriched at active enhancers associated with AR binding sites. Reflecting a significant genomic role for RARG to regulate androgen signaling, RARG knockdown in HPr1-AR cells significantly regulated the magnitude of the AR transcriptome. RARG down-regulation was explained by increased miR-96 in PCa cell and mouse models, and TCGA PCa cohorts. Biochemical approaches confirmed that miR-96 directly regulated RARG expression and function. Capture of the miR-96 targetome by biotin-miR96 identified that RARG and a number of RARG interacting co-factors including TACC1 were all targeted by miR-96, and expression of these genes were prominently altered, positively and negatively, in the TCGA-PRAD cohort. Differential gene expression analyses between tumors in the TCGA-PRAD cohort with lower quartile expression levels of RARG and TACC1 and upper quartile miR-96, compared to the reverse, identified a gene network including several RARG target genes (e.g. SOX15) that significantly associated with worse disease free survival (hazard ratio 2.23, 95% CI 1.58 to 2.88, p=0.015). In summary, miR-96 targets a RARG network to govern AR signaling, PCa progression and disease outcome. RWPE-1 non-malignant prostate cell line +/- 30nM bi-NC or bi-96, Pulldown & Input (24 hr post-transfection)

2018-07-20 | GSE117103 | GEO

The miR-96 and RARG signaling axis governs androgen signaling and prostate cancer progression II

Project description:Expression levels of retinoic acid receptor gamma (NR1B3/RARG, encodes RARG), are commonly reduced in prostate cancer (PCa). Therefore we sought to establish the cellular and gene regulatory consequences of reduced RARG expression, and determine RARG regulatory mechanisms. RARG shRNA approaches in non-malignant (RWPE-1 and HPr1-AR) and malignant (LNCaP) prostate models revealed that reducing RARG levels, rather than adding exogenous retinoid ligand, had the greatest impact on prostate cell viability and gene expression. ChIP-Seq defined the RARG cistrome which was significantly enriched at active enhancers associated with AR binding sites. Reflecting a significant genomic role for RARG to regulate androgen signaling, RARG knockdown in HPr1-AR cells significantly regulated the magnitude of the AR transcriptome. RARG down-regulation was explained by increased miR-96 in PCa cell and mouse models, and TCGA PCa cohorts. Biochemical approaches confirmed that miR-96 directly regulated RARG expression and function. Capture of the miR-96 targetome by biotin-miR96 identified that RARG and a number of RARG interacting co-factors including TACC1 were all targeted by miR-96, and expression of these genes were prominently altered, positively and negatively, in the TCGA-PRAD cohort. Differential gene expression analyses between tumors in the TCGA-PRAD cohort with lower quartile expression levels of RARG and TACC1 and upper quartile miR-96, compared to the reverse, identified a gene network including several RARG target genes (e.g. SOX15) that significantly associated with worse disease free survival (hazard ratio 2.23, 95% CI 1.58 to 2.88, p=0.015). In summary, miR-96 targets a RARG network to govern AR signaling, PCa progression and disease outcome. LNCaP malignant prostate cell line +/- shRARG, +/- 250nM CD437 for 24 hours

2018-07-20 | GSE117102 | GEO

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