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Expression data after BCLAF1-L knockdown in human RKO cells

ABSTRACT: Bcl-2-accociated transcription factor 1(BCLAF1) has been reported to be involved in diverse biological processes. Alternative splicing leads to mutiple transcript virants in human cells and we are interested in functions of its full length isoform(BCLAF1-L) in human colon cancer cells, thus to understanding its role in colon cancer progression. We used microarray to detail the global programme of gene expression after BCLAF1-L knockdown(sh-BCLAF1-L#1) in RKO cells and identified distinct classes of up-regulated or down-regulated genes impaired by its inhibition, when comparing with the control group(sh-Luci).

ORGANISM(S): Homo sapiens

PROVIDER: GSE52990 | GEO | 2013/12/05

SECONDARY ACCESSION(S): PRJNA230635

REPOSITORIES: GEO

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Expression data after BCLAF1-L knockdown in human RKO cells

Project description:Bcl-2-accociated transcription factor 1(BCLAF1) has been reported to be involved in diverse biological processes. Alternative splicing leads to mutiple transcript virants in human cells and we are interested in functions of its full length isoform(BCLAF1-L) in human colon cancer cells, thus to understanding its role in colon cancer progression. We used microarray to detail the global programme of gene expression after BCLAF1-L knockdown(sh-BCLAF1-L#1) in RKO cells and identified distinct classes of up-regulated or down-regulated genes impaired by its inhibition, when comparing with the control group(sh-Luci). RKO cells were infected with retroviruses either expressing control (sh-Luci) or BCLAF1-L knockdown (sh-BCLAF1-L#1). Medium was replaced 24h after infection, and infected cells were selected by the addition of puromycin (2ug/ml) for 72-96h. Then cells were havested for RNA extraction and hybridization on Affymetrix microarrays.

2013-12-05 | E-GEOD-52990 | biostudies-arrayexpress

BCLAF1 and its pre-mRNA splicing regulator SRSF10 both regulate tumorigenic capacity of human colon cancer cells

Project description:Bcl-2-accociated transcription factor 1(BCLAF1) has been shown to be involved in multiple biological processes. Transcript variants encoding different isoforms that are generated by alternative splicing have been found for this gene, but little is known about the mechanisms governing its splicing regulation and whether the misregulation is associated with cancer development. Mechanistic analysis revealed that splicing factor SRSF10 specifically interacts with exon5a and activates its inclusion, as RNAi-mediated knockdown of SRSF10 induced a dramatic skipping of exon5a. To define a comprehensive programm of alternative splicing that is regulated by SRSF10 in RKO cells, we used RNA-seq coupled with a bioinformatic analysis to identify the extensive splicing network regulated by SRSF10 in RKO cells.

2015-04-02 | GSE57325 | GEO

Expression data from RKO cells transfected with SPARCL1 and vector control

2011-09-30 | GSE31440 | GEO

Expression data from RKO cells transfected with SPARCL1 and vector control

Project description:Colon cancer cell line RKO grown on Matrigel form a luminal-like structure after the transfection of SPARCL1 gene, which may imply the differentiation of the cells. To indentify genes regulated by SPARCL1, we built two stable cell lines: RKO with pLXSN-SPARCL1 plasmid (RKO-SPARCL1) and RKO with pLXSN plasmid (RKO-pLXSN). Then we cultured these two cell lines on both plastic dish and dish cover with a layer of Matrigel. We used microarrays to undentify global gene expression change in RKO cells after the tranfection of SPARCL1. Four samples including RKO-pLXSN cells cultured on plastic, RKO-pLXSN cells cultured on Matrigel, RKO-SPARCL1 cells cultured on plastic and RKO-SPARCL1 cells cultured on Matrigel were trypsinized and collected for RNA extraction and hybridization on Affymetrix microarray U133plus2.0. Supplementary files: * RLvsRP: up and down regulated genes comparing with RKO-SPARCL1(RL) and RKO-pLXSN(RP) cells cultured on plastic * RLMvsRPM: up and down regulated genes comparing with RKO-SPARCL1(RL) and RKO-pLXSN(RP) cells cultured on Matrigel

2011-09-29 | E-GEOD-31440 | biostudies-arrayexpress

Mediator MED23 induces premature senescence by interacting with BCLAF1 via blocking autophagy flux in lung cancer cells

Project description:macroautophagy/autophagy plays a key role in regulating the balance between cell survival and senescence during the progression of lung cancer. Med23 (also known as Sur2), a protein belonging to an evolutionarily conserved high-molecularmass complex composed of more than 20 distinct subunits, promotes the growth, metastasis , and migration of lung cancer cells and is overexpressed in multiple cancers. However, the function of MED23 in autophagy regulation remains unknown. Here, we observes that MED23 expression is significantly upregulated in a subset of cancer cells and reversely correlated with overall survival rates and clinical stage for lung cancer patients. Mechanistically, MED23 is found to interact with BCLAF1 (BCL-2-associated transcription factor 1, BTF) ,a nuclear protein that can induce apoptosis and autophagy. Moreover, BCLAF1 interacts with the promoter of NUPR1 and downregulates its expression. We further show that BCLAF1 and MED23 depletion inhibits autophagy and induces premature senescence in vitro. Remarkably, the expression of BCLAF1 and MED23 are negatively correlated with NUPR1 in the human lung cancer tissues and adjacent normal tissues. Collectively, our data reveal a physical and genetic interaction between BCLAF1 and MED23, suggesting that MED23 constitutes a molecular node in the regulatory network of autophagy and this pathway may be an important therapeutic target in lung cancer.

2019-12-23 | GSE142508 | GEO

Effect of coculture with normal colonic epithelial cells on gene expression of RKO colon cancer cells

Project description:To investigate the effect of extracellular vesicle-treated normal colonic epithelial cells (FHC) on the activities of oncogenic signaling pathways in colon cancer cells (RKO), RKO cells were cocultured with FHC cells prestimulated with extracellular vesicles (EVs) or PBS.

2023-05-24 | GSE233326 | GEO

DNMT3B targets in RKO cells by ChIP-on-chip

Project description:Chromatin immunoprecipitation with DNMT3B specific antibody followed by CGI microarray identified genes with or without CGIs, repeat elements and genomic contigs in RKO cells. ChIP-Chop analysis showed that majority of the target genes including P16, DCC, DISC1, SLIT1, CAVEOLIN1, TBX5, TBX18, HOXB13 and some histone variants, that harbor CGI in their promoters, were methylated in multiple colon cancer cell lines but not in normal colon epithelial cells. Further, these genes were reactivated in RKO cells after treatment with 5-aza-2â-deoxycytidine, a DNA hypomethylating agent. COBRA and bisulfite genomic sequencing showed that the CGIs encompassing the transcription start sites (TSS) of DCC, TBX5, TBX18, SLIT1 were also methylated in primary colorectal tumors compared to matching normal tissues whereas GNA11 was methylated in both. MassARRAY analysis demonstrated that the CGI located ~4.5 kb upstream of HOXB13 +1 site was tumor-specifically hypermethylated in primary colorectal cancers and cancer cell lines. Analysis of tumor suppressor properties of two aberrantly methylated transcription factors, HOXB13 and TBX18, revealed that both inhibited growth and clonogenic survival of colon cancer cells in vitro, but only HOXB13 abolished tumor growth in nude mice. Chromatin immunoprecipitation with DNMT3B specific antibody in RKO cells was compared to control antibody.

2010-05-06 | E-GEOD-18929 | biostudies-arrayexpress

RNAi knock down of SIM2s in human RKO colon carcinoma cells in a timecourse

Project description:RKO Colon Carcinoma Cells were treated with 100nM of either SIM2s Control or Antisense oligos in a timecourse (10, 14, 18, 24hr) dependent manner.

2004-11-01 | E-MEXP-101 | biostudies-arrayexpress

DNMT3B targets in RKO cells by ChIP-on-chip

Project description:Chromatin immunoprecipitation with DNMT3B specific antibody followed by CGI microarray identified genes with or without CGIs, repeat elements and genomic contigs in RKO cells. ChIP-Chop analysis showed that majority of the target genes including P16, DCC, DISC1, SLIT1, CAVEOLIN1, TBX5, TBX18, HOXB13 and some histone variants, that harbor CGI in their promoters, were methylated in multiple colon cancer cell lines but not in normal colon epithelial cells. Further, these genes were reactivated in RKO cells after treatment with 5-aza-2’-deoxycytidine, a DNA hypomethylating agent. COBRA and bisulfite genomic sequencing showed that the CGIs encompassing the transcription start sites (TSS) of DCC, TBX5, TBX18, SLIT1 were also methylated in primary colorectal tumors compared to matching normal tissues whereas GNA11 was methylated in both. MassARRAY analysis demonstrated that the CGI located ~4.5 kb upstream of HOXB13 +1 site was tumor-specifically hypermethylated in primary colorectal cancers and cancer cell lines. Analysis of tumor suppressor properties of two aberrantly methylated transcription factors, HOXB13 and TBX18, revealed that both inhibited growth and clonogenic survival of colon cancer cells in vitro, but only HOXB13 abolished tumor growth in nude mice.

2010-03-01 | GSE18929 | GEO

BCLAF1 Chip-chip control (siGFP) and BRCA1 depleted (siBRCA1) 293T cells in the absense or presense of Etoposide

Project description:BCLAF1 is a serine-arginine (SR) protein implicated in transcriptional regulation and mRNA splicing. We have recently identified BCLAF1 as part of a novel mRNA splicing complex that is recruited to different genetic promoters by the breast cancer susceptiblity protein, BRCA1 in response to DNA damage. This ChIP-chip study was designed to identify genes/promoters regulated by the BRCA1/BCLAG1 mRNA splicing complex by identifying promoters bound by BCLAF1 in the absense and presense of BRCA1 in control cells and cells treated with etoposide to induce DNA damage. This study includes tripicate BCLAF1 ChIP-chip experiments in untreated and etoposide treated (1uM 16 hours) control cells (siGFP) and cells depleted of BRCA1 (siBRCA1). Chromatin Immunoprecipitaitons were performed in triplicate with BCLAF1 antibodies in control 293T cells transfected with siGFP siRNAs and BRCA1 siRNAs (siBRCA1 to deplete BRCA1). Immunoprecipitated genomic DNA was labelled with Cy3 and Input genomic DNA was labelled with Cy5 and hybridized to NimbleGen human 3x720k RefSeq promoter arrays to identify BCLAF1 boundgenomic DNA regions.

2014-04-25 | E-GEOD-47016 | biostudies-arrayexpress

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