SOX2 Genomic Localization in Small Cell Lung Cancer Cell Lines
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA757626 | ENA |
REPOSITORIES: ENA
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Project description:We utilized CUT&RUN to assess the genome-wide binding of SOX2 in human small cell lung cancer cell lines.
2021-12-02 | GSE182728 | GEO
Project description:SOX2 is a lineage specifier oncogene for lung squamous cell carcinoma (LSCC) and frequently amplified and overexpressed in human LSCC tumors (up to 90% of the cases). Our study demonstrated that SOX2 is a key determinant of neutrophil recruitment to tumors even in the absence of squamous histology. We generated cell lines from KrasLSL-G12D/+;Trp53fl/fl (KP) tumors that overexpress Sox2 (i.e. tumors from Lenti-Sox2-Cre infected KP mice that are validated to have Sox2 overexpression) (abbreviated as KPS) and employed chromatin immunoprecipitation sequencing (ChIP-seq) to identify genomic binding loci of SOX2 in KPS lines as well as Lkb1fl/fl;Ptenfl/fl (LP) LSCC tumors.
2018-10-16 | GSE118244 | GEO
Project description:SOX2 genomic binding sites in lung squamous cell carcinoma GEMM tumor and cell lines
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Project description:SOX2 is a transcription factor essential for self-renewal and pluripotency of embryonic stem cells. Recently SOX2 was found overexpressed in the majority of the lung squamous cell carcinoma (SQC), in which it acts as a lineage-survival oncogene. However, downstream targets/pathways of SOX2 in lung SQC cells remain to be identified. In order to identify genes/pathways likely to be downstream of SOX2, we conducted SOX2 silencing experiments in LK2 and NCI-H520 (H520 thereafter), two SOX2-abundant lung SQC cell lines and analyzed global gene transcription changes by gene expression microarray assay.
2014-07-30 | GSE48871 | GEO
Project description:SOX2 is a transcription factor essential for self-renewal and pluripotency of embryonic stem cells. Recently SOX2 was found overexpressed in the majority of the lung squamous cell carcinoma (SQC), in which it acts as a lineage-survival oncogene. However, downstream targets/pathways of SOX2 in lung SQC cells remain to be identified. In order to identify genes/pathways likely to be downstream of SOX2, we conducted SOX2 silencing experiments in LK2 and NCI-H520 (H520 thereafter), two SOX2-abundant lung SQC cell lines and analyzed global gene transcription changes by gene expression microarray assay. Each of H520 and LK2 cell lines was treated with either pooled siRNAs of SOX2 or non-silencing (control) siRNAs. After 48 h, cells were harvested and totoal RNA extracted for gene expression microarray analysis using Illumina HumanHT12 v3 BeadChip.
2014-07-30 | E-GEOD-48871 | biostudies-arrayexpress
Project description:Sox2 has been studied in several types of human solid tumors. The investigators found that Sox2 had higher expression level in colorectal cancer and metastatic tissues than normal tissues. So the investigators assumed that whether Sox2 plays an important role in the progression and migration of colon cancer.
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Project description: Not available
| S-EPMC3557461 | biostudies-literature
Project description:Cellular differentiation requires cells to undergo dramatic but strictly controlled changes in chromatin organization, transcriptional regulation, and protein production and interaction. To understand the regulatory connections between these processes, we applied a multi-omics approach integrating proteomic, transcriptomic, chromatin accessibility, protein occupancy, and protein-chromatin interaction data acquired during differentiation of mouse embryonic stem cells (ESCs) into post-mitotic neurons. We found extensive remodeling of the chromatin that was preceding changes on RNA and protein levels. We found the pluripotency factor Sox2 as regulator of neuron-specific genes and, as a potential mechanism, revealed its genomic redistribution from pluripotency enhancers to neuronal promoters and concomitant change of its protein interaction network upon differentiation. We identified Atrx as a major Sox2 partner in neurons, whose co-localisation correlated with an increase in active enhancer marks and increased expression of nearby genes, and where deletion of a Sox2-Atrx co-bound site resulted in reduced expression of the proximal gene. Collectively, these findings provide key insights into the regulatory transformation of Sox2 during neuronal differentiation and highlight the significance of multi-omic approaches in understanding gene regulation in complex systems.
2020-06-04 | PXD016080 | Pride
Project description:SOX2 is a transcription factor essential for pluripotent stem cells, and development and maintenance of squamous epithelium. We previously reported SOX2 an oncogene subject to highly recurrent genomic amplification in squamous cell carcinomas (SCCs). Here we demonstrate in SCCs that SOX2 interacts with another master squamous transcription factor p63, and through ChIP-seq show that genomic occupancy of SOX2 overlaps with that of p63 at a large number of loci and that they cooperatively regulate gene expression including ETV4, which we find essential for SOX2-amplified SCC cell survival. Furthermore, SOX2 binds to distinct genomic loci in SCCs than in embryonic stem cells and the SOX2-p63 coordinate binding is unique to SCC. In addition, a subset of SOX2 genomic binding sites in SCC that lack p63 co-occupancy are co-occupied by the AP-1 transcriptional complex. These demonstrate that SOX2’s actions in SCC differ substantially from its role in pluripotency and identify novel SOX2 interactions that will enable deeper characterization of SOX2’s function in SCC. SOX2 and p63 ChIP-seq from three lung and esophageal squamous carcinoma cell lines with amplification of SOX2 as well as SOX2 ChIP-seq from an ES cells.
2014-03-12 | E-GEOD-46837 | biostudies-arrayexpress
Project description:SOX2 is a transcription factor essential for pluripotent stem cells, and development and maintenance of squamous epithelium. We previously reported SOX2 an oncogene subject to highly recurrent genomic amplification in squamous cell carcinomas (SCCs). Here we demonstrate in SCCs that SOX2 interacts with another master squamous transcription factor p63, and through ChIP-seq show that genomic occupancy of SOX2 overlaps with that of p63 at a large number of loci and that they cooperatively regulate gene expression including ETV4, which we find essential for SOX2-amplified SCC cell survival. Furthermore, SOX2 binds to distinct genomic loci in SCCs than in embryonic stem cells and the SOX2-p63 coordinate binding is unique to SCC. In addition, a subset of SOX2 genomic binding sites in SCC that lack p63 co-occupancy are co-occupied by the AP-1 transcriptional complex. These demonstrate that SOX2’s actions in SCC differ substantially from its role in pluripotency and identify novel SOX2 interactions that will enable deeper characterization of SOX2’s function in SCC.
2014-03-12 | GSE46837 | GEO