Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA149345 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR354040_1.fastq.gz | Fastqsanger.gz | |||
| SRR354040_2.fastq.gz | Fastqsanger.gz | |||
| SRR354041_1.fastq.gz | Fastqsanger.gz | |||
| SRR354041_2.fastq.gz | Fastqsanger.gz | |||
| SRR354042_1.fastq.gz | Fastqsanger.gz |
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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
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Project description:Oncogenic BRAFV600E remodels the melanocyte transcriptome and induces BANCR to regulate melanoma cell migration
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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
Project description:To investigate whether cutaneous melanoma originates from a resident adult melanocyte stem cell (MSC) or a mature melanocyte, we created a model that recapitulates key histopathological features of human melanomagenesis by inducing a BRafV600E-driven melanomagenic program in interfollicular (IF) melanocytes located in mouse tails. To this end, we sequenced the transcriptome of FACS-sorted individual IFE reporter-positive cells from BRaf/Pten/tdTomato mice, the tails of which had been painted with 4-HT for 31 and 72 days, respectively. These time points were chosen as melanoma cells are exclusively found in the IF epidermis at day 31 (d31) and in both epidermis and dermis at day 72 (d72). Normal IF melanocytes from Tyr::CreERT2/+; ROSA26RLSL-tdTomato/+ were also isolated and profiled These data indicated that loss of differentiation markers occurs in a subset of targeted epidermal melanoma cells before the onset of dermal invasion and that this event may, at least partly, be a consequence of induction of Zeb1 expression.
2017-11-16 | GSE100607 | GEO
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 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.
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Project description:Malignant melanoma is characterized by frequent metastasis, however specific changes that regulate this process have not been clearly delineated. Although it is well known that Wnt signaling is frequently dysregulated in melanoma, the functional implications of this observation are unclear. By modulating beta-catenin levels in a mouse model of melanoma that is based on melanocyte-specific Pten loss and BrafV600E mutation, we demonstrate that beta-catenin is a central mediator of melanoma metastasis to lymph node and lung. In addition to altering metastasis, beta-catenin levels control tumor differentiation and regulate both MAPK/Erk and PI3K/Akt signaling. Highly metastatic tumors with beta-catenin stabilization are very similar to a subset of human melanomas; together these findings establish Wnt signaling as a metastasis regulator in melanoma. MoGene-1_0-st-v1: Four samples total. Two biological replicates of uncultured Pten/Braf murine melanomas and two biological replicates of uncultured Pten/Braf/Bcat-STA murine melanomas. MoEx-1_0-st-v1: Two samples total. Dissociated tumor and FACS-enriched Pten/Braf and Pten/Braf/Bcat-STA murine melanoma.
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Project description:Somatic oncogenic mutation of BRAF coupled with inactivation of PTEN constitute a frequent combination of genomic alterations driving development of human melanoma. Mice genetically engineered to conditionally express oncogenic BrafV600E and inactivate Pten in melanocytes following tamoxifen treatment rapidly develop melanoma. While early stage melanomas comprised melanin-pigmented Mitf and Dct-expressing cells, expression of these and other melanocyte identity genes was lost in later stage tumours that showed histological and molecular characteristics of de-differentiated neural crest type cells. Melanocyte identity genes displayed loss of active chromatin marks and RNA polymerase II and gain of heterochromatin marks indicating epigenetic reprogramming during tumour progression. Nevertheless, late stage tumour cells grown in culture re-expressed Mitf and melanocyte markers and Mitf together with Sox10 co-regulated a large number of genes essential for their growth. In this melanoma model, somatic inactivation that the catalytic Brg1 (Smarca4) subunit of the SWI/SNF complex and the scaffolding Bptf subunit of the NuRF delayed tumour formation and deregulated large and overlapping gene expression programs essential for normal tumour cell growth. Moreover, we show that Brg1 and Bptf co-regulated many genes together with Mitf and Sox10. Together these transcription factors and chromatin remodelling complexes orchestrate essential gene expression programs in mouse melanoma cells
2019-04-17 | GSE100998 | GEO
Project description:Malignant melanoma is characterized by frequent metastasis, however specific changes that regulate this process have not been clearly delineated. Although it is well known that Wnt signaling is frequently dysregulated in melanoma, the functional implications of this observation are unclear. By modulating beta-catenin levels in a mouse model of melanoma that is based on melanocyte-specific Pten loss and BrafV600E mutation, we demonstrate that beta-catenin is a central mediator of melanoma metastasis to lymph node and lung. In addition to altering metastasis, beta-catenin levels control tumor differentiation and regulate both MAPK/Erk and PI3K/Akt signaling. Highly metastatic tumors with beta-catenin stabilization are very similar to a subset of human melanomas; together these findings establish Wnt signaling as a metastasis regulator in melanoma.
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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
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