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ABSTRACT: The identification of RBM47 binding sites and RBM47-dependent alternative splicing events in brain metastatic breast cancer cells

OTHER RELATED OMICS DATASETS IN: E-GEOD-58379

PROVIDER: PRJNA252381 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1374810_1.fastq.gz	Fastqsanger.gz
	SRR1374810_2.fastq.gz	Fastqsanger.gz
	SRR1374811_1.fastq.gz	Fastqsanger.gz
	SRR1374811_2.fastq.gz	Fastqsanger.gz
	SRR1374812_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Identification of alternatively spliced transcripts in brain metastatic derivatives of MDA-MB-231 breast cancer cells in response to RBM47 expression

Project description:Changes in alternative splicing in breast cancer cells expressing control, empty vector or Flag-tagged wild type RBM47 were analyzed using paired-end, 100bp RNAseq. Related data published together with these data are found in GSE53779 Triplicate RNAseq libraries were prepared from non-clonal brain metastatic breast cancer cells stably expressing empty-vector, and a clonal cell line (wt#10) expressing Flag-tagged, wild-type RBM47 under a doxycline-inducible promoter, both treated for three days with doxycycline to induce transgene expression

2014-06-11 | E-GEOD-58379 | biostudies-arrayexpress

Flag-RBM47 HITS-CLIP in brain metastatic derivatives of MDA-MB-231

Project description:Brain metastatic breast cancer cells were subjected to HITS-CLIP to identify the targets of the RNA binding protein RBM47 MDA231-BrM2a is characterized in PMID: 19421193; Related data published together with these data are found in GSE53779 Non-clonal brain metastatic breast cancer cells stably expressing Flag-tagged, wild-type RBM47 under a doxycline-inducible promoter were treated for three days with doxycycline then UV-irradiated and subjected to Flag HITS-CLIP

2014-06-11 | E-GEOD-58380 | biostudies-arrayexpress

Determination of a comprehensive alternative splicing regulatory network and the combinatorial regulation by key factors during Epithelial-to-Mesenchymal Transition [RBM47 KD]

2016-04-05 | GSE75491 | GEO

RNA-binding Motif Protein RBM47 Promotes Tumorigenesis in Nasopharyngeal Carcinoma through Multiple Pathways

Project description:ABSTRACT RNA binding motif proteins (RBMs) have been widely implicated in the tumorigenesis of multiple human cancers, but scarcely studied in nasopharyngeal carcinoma (NPC). Here, we compare the mRNA levels of 29 RBMs between 87 NPC and 10 control samples. We find that RBM47 is frequently upregulated in NPC specimens and its high expression is associated with poor prognosis of patients with NPC. Biological experiments show that RBM47 plays an oncogenic role in NPC cells. Mechanically, RBM47 binds to the promoter and regulates the transcription of BCAT1 and its overexpression partially rescues the inhibitory effects of RBM47-knockdown on NPC cells. Moreover, transcriptome analysis reveals that RBM47 regulates alternative splicing of pre-mRNA, including those cancer-related, to a large extent in NPC cells. Furthermore, RBM47 binds to hnRNPM and cooperativelyjointly regulates multiple splicing events in NPC cells. In addition, we find that knockdown of hnRNPM inhibits proliferation and migration of NPC cells. Taken together, our study shows that RBM47 promotes the progression of NPC through multiple pathways, acting as a transcriptional factor and a modulator of alternative splicing in cooperation with hnRNPM. Our study also highlights that RBM47 and hnRNPM could be prognostic factors and potential therapeutic targets for NPC. Keywords RBM47, BCAT1, Alternative splicing, hnRNPM, Nasopharyngeal Carcinoma (NPC)

2022-06-01 | GSE176549 | GEO

Determination of a comprehensive alternative splicing regulatory network and the combinatorial regulation by key factors during Epithelial-to-Mesenchymal Transition [RBM47 KD]

Project description:RBM47 is a RNA binding protein that is known to regulate alternative splicing. To study the genome wide regulatory role of RBM47 in alternative splicing and determine the potential function of RBM47 during EMT, we used lentiviral shRNAs to knockdown RBM47 in H358 cells and performed RNA-seq in biological triplicates. We used lentiviral based shRNAs to knockdown RBM47 in human H358 cells. We harvested total RNA and protein from RBM47 knockdown and control knockdown in biological triplicates. We made cDNA libraries for each replicate and subjected them to RNA-seq.

2016-04-05 | E-GEOD-75491 | biostudies-arrayexpress

Flag-RBM47 HITS-CLIP in brain metastatic derivatives of MDA-MB-231

2014-06-11 | GSE58380 | GEO

The RNA-binding protein RBM47 suppresses metastatic breast cancer progression

Project description:Through integrative analysis of clinical breast cancer gene expression datasets, cell line models of breast cancer progression, and mutation data from cancer genome resequencing studies, we have identified RNA binding motif protein 47 (RBM47) as a candidate suppressor of breast cancer metastasis. RBM47 inhibited breast cancer progression in experimental models. Transcriptome-wide analysis of RBM47 localization by HITS-CLIP revealed widespread binding to mRNAs, preferentially at the 3' UTRs. RBM47 altered the abundance of a subset of its target mRNAs. Some of the mRNAs stabilized by RBM47, as exemplified by dickkopf WNT signaling pathway inhibitor 1 (DKK1), mediate tumor suppressive effects downstream of RBM47. This work identifies RBM47 as a suppressor of breast cancer progression and highlights the potential of global RNA modulatory events as a source of metastasis-promoting phenotypic traits. Cancer cells transduced with doxycycline-inducible wildtype RBM47 or the RBM47-I281fs mutant, treated with increasing concentrations of doxycycline.

2014-06-11 | E-GEOD-53779 | biostudies-arrayexpress

The RNA-binding protein RBM47 suppresses metastatic breast cancer progression

2014-06-11 | GSE53779 | GEO

Identification of alternatively spliced transcripts in brain metastatic derivatives of MDA-MB-231 breast cancer cells in response to RBM47 expression

2014-06-11 | GSE58379 | GEO

Co-regulation of alternative splicing by hnRNPM and ESRP1 during EMT

Project description:The epithelial-mesenchymal transition (EMT) is a fundamental developmental process that is abnormally activated in cancer metastasis. Dynamic changes in alternative splicing occur during EMT. ESRP1 and hnRNPM are splicing regulators that promote an epithelial splicing program and a mesenchymal splicing program, respectively. The functional relationships between these splicing factors in the genome-scale remain elusive. Comparing alternative splicing targets of hnRNPM and ESRP1 revealed that they co-regulate a set of cassette exon events, with the majority showing discordant splicing regulation. hnRNPM discordantly regulated splicing events show a positive correlation with splicing during EMT while concordant splicing events do not, highlighting the antagonistic role of hnRNPM and ESRP1 during EMT. Motif enrichment analysis near co-regulated exons identifies guanine-uridine rich motifs downstream of hnRNPM-repressed and ESRP1-enhanced exons, supporting a model of competitive binding to these cis-elements to antagonize alternative splicing. The set of co-regulated exons are enriched in genes associated with cell-migration and cytoskeletal reorganization, which are pathways associated with EMT. Splicing levels of co-regulated exons are associated with breast cancer patient survival and correlate with gene sets involved in EMT and breast cancer subtypes. In conclusion, hnRNPM and ESRP1 co-regulate antagonistically a set of alternative splicing events that occur during EMT. This regulation is likely mediated through competition for the same intronic binding sites downstream of variable exons. hnRNPM and ESRP1 regulated splicing events are associated with breast cancer survival.

2018-08-01 | GSE112516 | GEO

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