RNA-seq analysis of SCC1 and FaDu cells after FOSL1 depletion
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA634840 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:In order to examine how FOSL1 affects the global gene transcriptome in HNSCC, we performed RNA-sequencing in SCC1 and FaDu cells treated with FOSL1 siRNA. Depletion of FOSL1 led to inhibition of cancer stemness genes.
2022-05-23 | GSE151128 | GEO
Project description:To explore genome-wide alteration MED1 and FOSL1 after depletion of FOSL1, we performed chromatin immunoprecipitation sequencing (ChIP-seq) of SCC1 cells to examine genome-wide recruitment of MED1 and FOSL1 following FOSL1 knockdown. Depletion of FOSL1 led to dramatically loss of the recruitment of MED1 and FOSL1 at a cohort of key oncogenes associate with tumorigenesis and metastasis.
2021-04-14 | GSE151132 | GEO
Project description:ChIP-seq analysis of MED1 and FOSL1 in SCC1 cells after depletion of FOSL1
| PRJNA634845 | ENA
Project description:Despite recent advances in genomic profiling techniques, the precise mechanisms controlling GBM subtypes and their plasticity are not fully unraveled. Here,using transcriptomic data of patient derived stem cell lines we found that FOSL1 is a master regulator of the MES subtype. Depletion of FOSL1 resulted in loss of themesenchymal gene signature (MGS) in mouse Kras-mutant neural stem cells and in human brain tumor stem cells.
2020-09-30 | GSE138010 | GEO
Project description:RNA-Seq of FaDu Cas9 isogenic cells treated with fractionated RT.
2021-03-07 | GSE147085 | GEO
Project description:Cisplatin is a common chemotherapeutic drug for hypopharyngeal cancer. But cisplatin-resistance of hypopharyngeal cancer is rarely explored. We cultured hypopharyngeal cancer cell (FaDu) and induced its cisplatin-resistant cell (FaDu/DDP4). The resistance index (RI) of FaDu/DDP4 was 2.828. Then we tested the differentially expressed genes (DEGs) between FaDu and FaDu/DDP4. DEGs contain 2388 lncRNAs, 1932 circRNAs, 745 mRNAs and 202 miRNAs. We used Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyzed the DEGs. The differentially expressed 745 mRNAs were classified into 3 domains and 47 secondary GO terms. In KEGG pathway enrichment, “TNF signaling pathway”, “IL-17 signaling pathway” and “JAK-STAT signaling pathway” have greater enrich factors. And we drew the ceRNA networks of DEGs. 52 lncRNAs, 148 circRNAs, 155 mRNAs and 18 miRNAs were selected to draw the network. We noticed several potential targets (as miR-197-5p, miR-6808-5p, APOE, MMP1, S100A9 and CYP24A1). At last, we chose 8 miRNAs and 6 mRNAs for qRT-PCR to verify our microarray. In them, miR-197-5p, miR-6808-5p, APOE, MMP1, S100A9 and CYP24A1 might be potential genes inducing resistance.
2021-06-02 | GSE167396 | GEO
Project description:The differentiation of Th17 cells is controlled by a complex network of transcription factors (TFs), including FOS and JUN proteins of the AP-1 family. The FOS-like proteins, FOSL1 and FOSL2 have recently been reported to control Th17 responses. The molecular mechanisms dictating their roles, however, are unclear. Moreover, although the functions of AP-1 TFs are largely governed by their protein-protein interactions, these are also poorly characterized in this milieu. Using affinity purification in combination with mass-spectrometry we established the first interactomes of FOSL1 and FOSL2 in human Th17 cells. In addition to their known interactions with JUN proteins, our analysis identified several novel binding partners of FOSL factors. Gene ontology analysis revealed RNA binding was enriched as the major functionality for FOSL1 and FOSL2 associated proteins, thereby suggesting possible mechanistic links that have not been studied before. Intriguingly, 29 interactors were found to be shared between FOSL1 and FOSL2, which included crucial regulators of Th17-fate. These findings, including unique and shared interactions, were validated using parallel reaction monitoring targeted mass-spectrometry (PRM-MS), with additional measurements with other laboratory methods. Overall, this study provides key insights into interaction-based signalling mechanisms of FOSL1 and FOSL2, which potentially control Th17 cell-development and associated pathologies.
2021-11-02 | PXD025729 | Pride
Project description:FaDu treated with citric buffer vs. rCTGF FaDu treated with citric buffer for 24 hours FaDu treated with rCTGF 100 ng/mL for 24 hours
2013-01-01 | E-GEOD-30423 | biostudies-arrayexpress
Project description:Cohesin is essential for genome folding and chromosome inheritance through cell divisions. In somatic cells, both of these functions are mediated by Scc1-cohesin, which in mitosis is released from chromosomes by Wapl and separase. In mammalian oocytes, cohesion is mediated by Rec8-cohesin. Scc1 is also expressed but neither required nor sufficient for cohesion, and its function in oocytes is unknown. Likewise, it is unknown whether Wapl regulates one or both cohesin complexes and chromosome segregation in mature oocytes. Using conditional mouse mutagenesis, we show that in meiosis I Wapl is required for proper chromosome segregation, predominantly releases Scc1-cohesin from chromosomes and promotes production of euploid eggs. Using single-nucleus Hi-C, we found that Scc1 is essential for chromatin loops and topologically associating domains (TADs) in oocytes. Increasing Scc1 residence time on chromosomes by Wapl depletion leads to vermicelli formation and intra-loop structures but, unlike in mitotic cells, does not increase loop size. This implies that loop size has reached a maximum in oocytes, possibly because it is limited by barriers such as cohesive cohesin. We conclude that distinct cohesin complexes generate loops and cohesion in mammalian oocytes and propose that the same principle applies to all cell types and species.
2020-03-04 | GSE132264 | GEO