Analysis of genes regulated by FoxD3 in B16-F10 mouse melanoma cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE13129 | GEO | 2008/10/15
SECONDARY ACCESSION(S): PRJNA109675
REPOSITORIES: GEO
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Project description:We wished to examine the genes regulated by FoxD3 in pigment cells to gain understanding in how FoxD3 represses melanoblast specification in the neural crest. For technical reasons, we could not use neural crest cells, so we used melanoma cells, since they are derived from neural crest cells. To this end, we transfected B16-F10 mouse melanoma cells with constructs expressing FoxD3, or FoxD3-VP16, in which the C-terminal portion of FoxD3 (which contains the transcriptional repression domain) has been replaced by the VP16 transcriptional activation domain. Experiment Overall Design: The base vector used for these studies was pMES, which expresses the gene of interest under control of the chick beta-actin promoter. EGFP is also expressed from the bicistronic mRNA through the use of an IRES. Experiment Overall Design: B16-F10 cells were transfected with either empty pMES, pFoxD3 (which contains FoxD3 inserted into pMES), or pFoxD3-VP16 (similar to pFoxD3, except that the C-terminal portion of FoxD3, which contains the transcriptional repression domain, has been replaced by the transcriptional activation domain of VP16). Experiment Overall Design: 24 hours after transfection, EGFP-positive cells were collected by FACS and those cells were subjected to microarray analysis.
2008-10-26 | E-GEOD-13129 | biostudies-arrayexpress
Project description:The neural crest (NC) is a transient embryonic stem cell population characterised by its multipotency and broad developmental potential. Here, we perform NC-specific transcriptional and epigenomic profiling of foxd3-mutant versus wild-type cells in vivo to define the gene regulatory circuits controlling NC specification. Together with global binding analysis obtained by foxd3 biotin-ChIP and single cell profiles of foxd3-expressing premigratory NC, our analysis shows that during early steps of NC formation, foxd3 acts globally as a pioneer factor to prime the onset of genes regulating NC specification and migration by re-arranging the chromatin landscape, opening cis-regulatory elements and reshuffling nucleosomes. Strikingly, foxd3 then gradually switches from an activator to its previously well-described role as a transcriptional repressor. Taken together, these results demonstrate that foxd3 acts bimodally in the neural crest as a switch from ‘permissive’ to ‘repressive’ nucleosome/chromatin organisation to maintain multipotency and define cell fates.
2018-12-07 | GSE106676 | GEO
Project description:The transcription factor forkhead box D3 (FoxD3) is a transcriptional factor which belongs to forkhead box (Fox) transcription factor family. The functions of FOXD3 in embryogenesis and in the development of neural crest cells have been clearly defined. Its tumor suppressor function hasbeen found in many types of cancer in recent years. However, the study about its roles in lung cancerdevelopment is still lacking. Our study found that deficiency of FoxD3 in lung cancer enhanced cell growth and cell invasion. RNA-sequence analysis demonstrated that loss of FoxD3 mainly affected cell cycle progression related gene expression. Knockdown of FoxD3 led to G2-M cell accumulation with up-regulation of DNA replication licensing factor MCM5 and MCM4 as well as cell cycle regulator polo-like kinase-1 (PLK1) and CDC6. Over-expression of those genesin lung cancer was associated with poor clinical outcomes of lung cancer patients. We also identified high mobility group box-1(HMGB1), Hras and Ephrin B1 gene expression increase after FoxD3 silencing which may participate in enhanced lung cancer cell invasion. Our study identifiedtumor suppressor function of FoxD3 in lung cancer andwe did the first comprehensive analysis of the genes regulated by FoxD3 for cell proliferation and invasion in lung cancer. The identified genes regulated by FoxD3 through our analysis will provide valuable information to uncover the mechanism of FoxD3 tumor suppressor function. Three control and three FOXD3 knockdown A549 cell lines were subjected to RNA sequencing.
2015-12-24 | E-GEOD-64513 | biostudies-arrayexpress
Project description:The transcription factor forkhead box D3 (FoxD3) is a transcriptional factor which belongs to forkhead box (Fox) transcription factor family. The functions of FOXD3 in embryogenesis and in the development of neural crest cells have been clearly defined. Its tumor suppressor function hasbeen found in many types of cancer in recent years. However, the study about its roles in lung cancerdevelopment is still lacking. Our study found that deficiency of FoxD3 in lung cancer enhanced cell growth and cell invasion. RNA-sequence analysis demonstrated that loss of FoxD3 mainly affected cell cycle progression related gene expression. Knockdown of FoxD3 led to G2-M cell accumulation with up-regulation of DNA replication licensing factor MCM5 and MCM4 as well as cell cycle regulator polo-like kinase-1 (PLK1) and CDC6. Over-expression of those genesin lung cancer was associated with poor clinical outcomes of lung cancer patients. We also identified high mobility group box-1(HMGB1), Hras and Ephrin B1 gene expression increase after FoxD3 silencing which may participate in enhanced lung cancer cell invasion. Our study identifiedtumor suppressor function of FoxD3 in lung cancer andwe did the first comprehensive analysis of the genes regulated by FoxD3 for cell proliferation and invasion in lung cancer. The identified genes regulated by FoxD3 through our analysis will provide valuable information to uncover the mechanism of FoxD3 tumor suppressor function.
2015-12-24 | GSE64513 | GEO
Project description:Neuroblastoma (NB), a malignant embryonic tumor arising from primitive neural crest cells, accounts for more than 7% of malignancies and around 15% of cancer-related mortality in childhood. Better elucidating the mechanisms of tumorigenesis and aggressiveness is important for improving the therapeutic efficiencies of NB. Through mining of publically available microarray datasets, we discovered a novel 963-bp lncRNA, named FOXD3 antisense RNA 1 (FOXD3-AS1), as an independent prognostic marker for favorable clinical outcome of NB patients. To investigate the mechanisms underlying the oncogenic functions of FOXD3-AS1, we employed the Illumina HiSeq PE125/PE150 as a discovery platform to analyze the transcriptome profiling changes of human BE(2)-C cells in response to stable over-expression of FOXD3-AS1. The results showed that stable over-expression of FOXD3-AS1 led to altered expression of 3191 human mRNAs, including 1542 up-regulated genes and 1650 down-regulated genes. Then we found the possible roles of these differentially regulated mRNAs in selected pathways including cell cycle/proliferation, apoptosis, and cytokine/chemokine responses by Bioinformatic analysis. Furthermore, we validated the RNA-seq results by real-time RT-PCR with high identity. Overall, our results provided fundamental information about the transcriptomic changes in response to FOXD3-AS1 over-expression in human NB cells, and these findings will help us understand the pathogenesis of NB.
2018-10-30 | GSE105016 | GEO
Project description:To understand the transcriptional impact of FOXD3 in melanoma cells, we utilized a microarray approach. We collected RNA from three unrelated mutant B-RAF melanoma cell lines (WM115, WM793, and A375) that were engineered to inducibly express FOXD3 or the control gene, ?-galactosidase (LacZ), after 5 days of transgene induction. This time point was chosen based on maximal phenotypic changes previously observed. Comparison of gene signatures between the 3 cell lines produced approximately 2,600 common genes differentially regulated by FOXD3-expressing cells compared to the LacZ controls. Three unrelated mutant B-RAF melanoma cell lines (WM115, WM793, and A375) were induced to express FOXD3 and compared against the same cell lines expressing the control gene, ?-galactosidase (LacZ).
2013-03-31 | E-GEOD-43962 | biostudies-arrayexpress
Project description:To understand the transcriptional impact of FOXD3 in melanoma cells, we utilized a microarray approach. We collected RNA from three unrelated mutant B-RAF melanoma cell lines (WM115, WM793, and A375) that were engineered to inducibly express FOXD3 or the control gene, β-galactosidase (LacZ), after 5 days of transgene induction. This time point was chosen based on maximal phenotypic changes previously observed. Comparison of gene signatures between the 3 cell lines produced approximately 2,600 common genes differentially regulated by FOXD3-expressing cells compared to the LacZ controls.
2013-03-31 | GSE43962 | GEO
Project description:FOXD3 is essential in embryonic stem cells, however the primary molecular mechanism is unclear. Here, we performed BioID to identify proteins collaborating with FOXD3 in protecting embryonic stem cell survival.
2023-05-08 | PXD035284 | Pride
Project description:RNA-sequencing of neural crest cells collected from Gt(foxd3:mCherry);Tg(sox10:mEGFP) embryos
2019-09-05 | GSE135237 | GEO
Project description:The tumor-initiating cells (TIC) are cell population that can initiate tumor, mediate drug resistance, and give rise to metastasis. FOXD3 is a forkhead box (Fox) transcription factor family that regulates the pluripotency of embryonic stem cell and tumorigenicity. However, it is unclear whether FOXD3 play any role in TIC and tumor metastasis. Here, we report that FOXD3 is down-regulated in tumor initiating cells and negatively correlated with higher histologic grades and positive lymph node metastasis. FOXD3 repress TIC expansion, cell migration, drug resistance and osteogenesis in vitro and in vivo. Mechanically, we found that FOXD3 repress a cohort of genes including SET and WDR5 and to regulate several TIC related signaling pathway. Moreover, SET and WDR5 was positively correlated with the CSC abundance and tumor progression. Besides, patients with high expression of SET and WDR5 presented a poorer overall survival. Collectively, our work defined that FOXD3-WDR5-SET axis that repress TIC accumulation and lung cancer progression.
2017-01-10 | GSE93323 | GEO