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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Oncogenic BRAFV600E remodels the melanocyte transcriptome and induces BLNCR1 to regulate melanoma cell migration [Affymetrix]

ABSTRACT: Most cancer genomics papers to date have focused on aberrations in genomic DNA and protein-coding transcripts. However, around 50% of transcripts have no coding potential and may exist as non-coding RNA. We performed RNA-seq in BRAFv600e melanoma skin cancer and on melanocytes over-expressing oncogenic BRAF to catalog transcriptome remodeling. We discovered that BRAF regulates expression of 1027 protein coding transcripts, 39 annotated lncRNAs and 70 novel transcripts. Many of the novel transcripts are lncRNAs. We used an indepenedent dataset to interrogate our novel transcripts and found that the novel lncRNA BLNCR1 is a BRAF-regulated lncRNA recurrently upregulated in melanoma. Knockdown of BLNCR1 impairs melanoma cell migration. To identify genes regulated by BLNCR1 we perrformed shRNA knockdown experiments using 2 independent shRNA sequences in col829 melanoma cells. RNA was then extracted for microarray analysis.

ORGANISM(S): Homo sapiens

SUBMITTER: Kun Qu

PROVIDER: E-GEOD-37132 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Oncogenic BRAFV600E remodels the melanocyte transcriptome and induces BANCR to regulate melanoma cell migration [HT-seq]

Project description:Most cancer genomics papers to date have focused on aberrations in genomic DNA and protein-coding transcripts. However, around 50% of transcripts have no coding potential and may exist as non-coding RNA. We performed RNA-seq in BRAFv600e melanoma skin cancer and on melanocytes over-expressing oncogenic BRAF to catalog transcriptome remodeling. We discovered that BRAF regulates expression of 1027 protein coding transcripts, 39 annotated lncRNAs and 70 novel transcripts. Many of the novel transcripts are lncRNAs. We used an indepenedent dataset to interrogate our novel transcripts and found that the novel lncRNA BANCR is a BRAF-regulated lncRNA recurrently upregulated in melanoma. Knockdown of BANCR impairs melanoma cell migration. Whole transcriptome RNA-seq followed assembly to Refseq/Gencode and de novo transcript assembly. RNA-seq performed on: 2 BRAFv600e melanomas, melanocytes+RFP control and melanocytes + BRAFv600e. We discovered protein-coding transcripts, annotated ncRNAs and novel transcripts (including lncRNAs) regulated by BRAFv600e also coordinately expressed in melanoma.

2012-04-28 | E-GEOD-33092 | biostudies-arrayexpress

Oncogenic BRAFV600E remodels the melanocyte transcriptome and induces BANCR to regulate melanoma cell migration [Affymetrix]

2012-04-28 | GSE37132 | GEO

Oncogenic BRAFV600E remodels the melanocyte transcriptome and induces BANCR to regulate melanoma cell migration [HT-seq]

2012-04-28 | GSE33092 | GEO

Oncogenic Ras regulated long non-coding RNA Orilnc1 in human cancer

Project description:Ras and its downstream cascades transmit cellular signals, resulting in increased transcription of a large number of genes involved in cell growth and division. Research on long non-coding transcripts regulated by the Ras signaling cascade is still in its infancy. Long non-coding RNAs (lncRNAs) are operationally defined as transcripts that are larger than 200 nt that do not appear to have protein-coding potential. Using a custom-designed lncRNA microarray, we identified a novel lncRNA (oncogenic Ras-induced lncRNA 1, Orilnc1) whose expression is significantly induced by activation of Ras. Further molecular studies demonstrated that the expression of Orilnc1 is regulated by the Ras-Raf-MEK-ERK signaling cascade via the transcriptional factor AP1. Importantly, Orilnc1 is highly expressed in BRAF mutant cancers such as BRAF-driven melanoma. Inhibition of Orilnc1 expression by small RNA interference (siRNA) significantly blocked tumor cell proliferation and growth in vitro and in vivo. Finally, we observed that blocking Orilnc1 reduced expression levels of cell cycle related genes such as Cyclin E1 and induced G1/S arrest in tumor cells. Taken together, Orilnc1 may function as a novel non-protein mediator to respond the Ras/Raf activation and could serve as a potential therapeutic target for RAS or BRAF-driven cancers such as melanoma.

2017-09-05 | GSE90044 | GEO

Comprehensive Identification of Soybean Long Non-coding RNAs Reveals a Subset of Small Peptide-Coding Transcripts

Project description:Long non-coding RNAs (lncRNAs) are defined as non-protein-coding transcripts that are at least 200 nucleotides long. They are known to play pivotal roles in regulating gene expression, especially during stress responses in plants. We used a large collection of in-house transcriptome data from various soybean (Glycine max and Glycine soja) tissues treated under different conditions to perform a comprehensive identification of soybean lncRNAs. We also retrieved publicly available soybean transcriptome data that were of sufficient quality and sequencing depth to enrich our analysis. In total, RNA-seq data of 332 samples were used for this analysis. An integrated reference-based, de novo transcript assembly was developed that identified ~69,000 lncRNA gene loci. We showed that lncRNAs are distinct from both protein-coding transcripts and genomic background noise in terms of length, number of exons, transposable element composition, and sequence conservation level across legume species. The tissue-specific and time-specific transcriptional responses of the lncRNA genes under some stress conditions may suggest their biological relevance. The transcription start sites of lncRNA gene loci tend to be close to their nearest protein-coding genes, and they may be transcriptionally related to the protein-coding genes, particularly for antisense and intronic lncRNAs. A previously unreported subset of small peptide-coding transcripts was identified from these lncRNA loci via tandem mass spectrometry, which paved the way for investigating their functional roles. Our results also highlight the current inadequacy of the bioinformatic definition of lncRNA, which excludes those lncRNA gene loci with small open reading frames (ORFs) from being regarded as protein-coding.

2020-01-09 | PXD014553 | Pride

Global identification of growth-related long non-coding RNAs in breast muscle of chicken

Project description:Long non-coding RNAs (lncRNAs) can have potential roles in development of tissues and organs. We selected breast muscle of fast-growing White Recessive Rock chicken (WRR) and slow-growing Xing Hua chicken (XH) to identify lncRNA transcripts by LncRNA-Seq. This study identified 21,993 novel lncRNAs. Among 7,339 differentially expressed lncRNAs, 723 up-regulated and 6,616 down-regulated lncRNAs were found in WRR compared with XH. Of them, five novel lncRNA were antisense transcripts for growth-related genes CACNA1D (unigene 14689_all), IL4I1 (unigene 15355_all), LEF-1 (unigene 19525_all) and FABP1 (unigenes 17536_all and 17537_all) respectively. Meanwhile, 12 other novel lncRNAs were found in the intron or downstream of some known growth-related genes (IGF1, IGF2BP2, IGF2BP3, CACNA1D, IL4I1, LEF-1 and FABP1). In addition, 4,043 SSRs and 200,049 SNPs were identified. Our data revealed the global lncRNA expression pattern in muscle tissue, and contributed a useful genomic resource towards studying the effects of lncRNAs in regulating chicken growth. Two RNA pool for WRR and XH strains

2014-06-24 | E-GEOD-58755 | biostudies-arrayexpress

MITF ChIP-seq in primary melanocyte and melanoma as a function of oncogenic BRAF

Project description:Thousands of enhancers are characterized in the human genome, yet few have been shown important in cancer. Inhibiting oncokinases, such as EGFR, ALK, HER2, and BRAF, is a mainstay of current cancer therapy but is hindered by innate drug resistance mediated by upregulation of the HGF receptor, MET. The mechanisms mediating such genomic responses to targeted therapy are unknown. Here, we identify lineage-specific MET enhancers for multiple common tumor types, including a melanoma lineage-specific MET enhancer that displays inducible chromatin looping and MET gene induction upon BRAF inhibition. Epigenomic analysis demonstrated that the melanocyte-specific transcription factor, MITF, mediates this enhancer function. Targeted genomic deletion (<7bp) of the MITF motif within the MET enhancer suppressed inducible chromatin looping and innate drug resistance, while maintaining MITF-dependent, inhibitor-induced melanoma cell differentiation. Epigenomic analysis can thus guide functional disruption of regulatory DNA to decouple pro- and anti-oncogenic functions of tumor lineage-enriched transcription factors mediating innate resistance to oncokinase therapy. MITF ChIP-seq was performed in primary human melanocytes with overexpression of BRAFV600E or a lentiviral control (RFP), and in COLO829 melanoma cells treated with DMSO, or PLX4032

2014-01-14 | E-GEOD-50681 | biostudies-arrayexpress

Oncogenic BRAFV600E remodels the melanocyte transcriptome and induces BLNCR1 to regulate melanoma cell migration

Project description:This SuperSeries is composed of the following subset Series: GSE33092: Oncogenic BRAFV600E remodels the melanocyte transcriptome and induces BLNCR1 to regulate melanoma cell migration [HT-seq] GSE37132: Oncogenic BRAFV600E remodels the melanocyte transcriptome and induces BLNCR1 to regulate melanoma cell migration [Affymetrix] Refer to individual Series

2012-04-27 | E-GEOD-37169 | biostudies-arrayexpress

COLO829 treatment with PLX4032 and/or MITF knockdown

Project description:Thousands of enhancers are characterized in the human genome, yet few have been shown important in cancer. Inhibiting oncokinases, such as EGFR, ALK, HER2, and BRAF, is a mainstay of current cancer therapy but is hindered by innate drug resistance mediated by upregulation of the HGF receptor, MET. The mechanisms mediating such genomic responses to targeted therapy are unknown. Here, we identify lineage-specific MET enhancers for multiple common tumor types, including a melanoma lineage-specific MET enhancer that displays inducible chromatin looping and MET gene induction upon BRAF inhibition. Epigenomic analysis demonstrated that the melanocyte-specific transcription factor, MITF, mediates this enhancer function. Targeted genomic deletion (<7bp) of the MITF motif within the MET enhancer suppressed inducible chromatin looping and innate drug resistance, while maintaining MITF-dependent, inhibitor-induced melanoma cell differentiation. Epigenomic analysis can thus guide functional disruption of regulatory DNA to decouple pro- and anti-oncogenic functions of tumor lineage-enriched transcription factors mediating innate resistance to oncokinase therapy. COLO829 human melanoma cell line harboring the BRAFV600E mutation was treated with BRAF inhibtior PLX4032 (Vemurafenib) and/or a hairpin against MITF

2014-01-14 | E-GEOD-50649 | biostudies-arrayexpress

Novel long non-coding RNAs are involved in cellular response to angiotensin II signaling

Project description:Angiotensin II (AngII) is a polypeptide hormone that plays a pivotal role in the regulation of blood pressure. In vascular smooth muscle cells (VSMCs), AngII signaling results in hypertrophy, proliferation, contraction, and migration, which ultimately promote atherosclerosis and hypertensive cardiovascular diseases. Recent studies have shown that fundamental biological processes such as cell proliferation and differentiation are mediated in part by the activities of long non-protein-coding RNAs (lncRNAs). In this study, we sought to identify lncRNAs that are involved in the response to AngII-signaling. Genome-wide analysis of de novo assembled transcripts from rat vascular smooth muscle cells (VSMCs) identified novel lncRNA as well as protein-coding transcripts which have not been previously annotated. The majority of the genomic loci from which these novel transcripts are transcribed are enriched for histone H3 lysine 4 trimethylation and histone H3 lysine 36 trimethylation, two chromatin modifications that are closely associated with actively transcribed regions, further supporting these as bona fide transcripts. Compared with previously annotated rat transcripts, these novel lncRNA transcripts, on average, are shorter in length and are less abundant, consistent with reports from mice and humans. Expression analyses of transcripts from control and AngII-stimulated VSMCs reveal that AngII signaling affects the abundance of both protein-coding transcripts as well as lncRNAs transcripts. Altogether, these data provide new insights into the global effects of AngII signaling and reveal potential novel therapeutic targets for treatment of AngII-associated cardiovascular diseases. RNA-sequencing of control and AngII (3hrs)-stimulated rVSMSCs. ChIP-sequencing of H3K4me3 and H3K36me3 in control and AngII (3hrs)-stimulated rVSMCs.

2013-06-30 | E-GEOD-38056 | biostudies-arrayexpress

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