Gene expression profiling of Sox2+ Patched1+/- medulloblastoma cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE48766 | GEO | 2016/07/08
SECONDARY ACCESSION(S): PRJNA211590
REPOSITORIES: GEO
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Project description:Induction of the transcription factor Sox2 from a doxycycline-inducible promoter in iSox2-DAOY medulloblastoma cells. Affymetrix microarrays were used to characterize the gene expression profile of iSox2-DAOY cells in the absence and presence of doxycycline. Human DAOY medulloblastoma cells were engineered to express epitope tagged Sox2 under the control of a doxycycline inducible promoter, to produce iSox2-DAOY cells. iSox2-DAOY cells were FACS sorted into CD133 low and high populations. The CD133 low population was cultured in the absence and presence of 0.5 µg/mL doxycycline for 24 hours. RNA was extracted from cells cultured without and with doxycycline, and was used for microarray analysis.
2012-08-25 | E-GEOD-36947 | biostudies-arrayexpress
Project description:Induction of the transcription factor Sox2 from a doxycycline-inducible promoter in iSox2-DAOY medulloblastoma cells. Affymetrix microarrays were used to characterize the gene expression profile of iSox2-DAOY cells in the absence and presence of doxycycline.
2012-08-25 | GSE36947 | GEO
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:A series of mouse models designed to mimic pediatric medulloblastoma types in humans were tested by microarray and compared to published human medulloblastoma data Myc-type tumors [dka201-203] were generated by orthotopic injection of Myc-infected cerebellar cells from Cdkn2c-/-, Trp53-/-, Atoh1-GFP mice into the cerebral cortex of immunocompromised nude mice. For Shh-type medulloblastomas [dka204-206], spontaneous medulloblastomas from [Cdkn2c-/-; Trp53Fl/Fl; Nestin-Cre] (Uziel et al.,2005 Genes Dev) were used. FACS-sorted GFP-positive [dka220-222] and GFP-negative [dka211, 212 and 219] populations were obtained from postnatal day 6 Cdkn2c-/-, Trp53-/-, Atoh1-GFP cerebella. Myc-type secondary tumors [dka223-225] were generated by orthotopic transplantation of cultured sphere cells from Myc-type primary tumors.
2012-02-29 | E-GEOD-33200 | biostudies-arrayexpress
Project description:The proto-oncogene MYCN is mis-expressed in various types of human brain tumors. To clarify how developmental and regional differences influence transformation, we transduced wild-type or mutationally-stabilized murine N-mycT58A into neural stem cells (NSCs) from perinatal murine cerebellum, brain stem and forebrain. Transplantation of Nmyc WT NSCs was insufficient for tumor formation. N-mycT58A cerebellar and brain stem NSCs generated medulloblastoma/primitive neuroectodermal tumors, whereas forebrain NSCs developed diffuse glioma. Expression analyses distinguished tumors generated from these different regions, with tumors from embryonic versus postnatal cerebellar NSCs demonstrating SHH-dependence and SHH-independence, respectively. These differences were regulated in-part by the transcription factor SOX9, activated in the SHH subclass of human medulloblastoma. Our results demonstrate context-dependent transformation of NSCs in response to a common oncogenic signal. 9 (total) orthotopic tumors generated from E16C, P0C, and P0F NSCs transduced with a mutation-stabilized N-Myc were compared to transduced (but not transplanted) NSCs, NSCs transduced with GFP, and cells derived from the orthotopic tumors. These were also compared to 5 normal P7 cerebella, and 32 medulloblastoma tumors from the GTML mouse model. A cell line derived from a tumor from the GTML mouse model is also included in the comparison.
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Project description:Salivary gland squamous cell carcinomas (SG-SCCs) are a rare type of head and neck cancers which are linked to poor prognosis. Due to their low frequencies, the molecular mechanisms responsible for their aggressiveness are poorly understood. In this work we studied the function of the phosphatase DUSP1, a negative regulator of MAPK activity, in controlling the progression of SG-SCCs. We generated DUSP1 KO clones in A253 human cells. These clones showed a reduced ability to grow in 2D, self-renew in ECM matrices and grow tumors in immunodeficient mice. This was caused by an overactivation of the stress and apoptosis kinase JNK1/2 in DUSP1-KO clones. Interestingly, RNAseq analysis revealed that the expression of SOX2, a well know self-renewal gene was decreased at the mRNA and protein level. Unexpectedly, CRISPR-KO of SOX2 did not recapitulate DUSP1-KO phenotype, and SOX2-null cells had an enhanced ability to self-renew and grow tumors in mice. Gene expression analysis demonstrated that SOX2-null cells have a decreased squamous differentiation profile -losing TP63 expression- and an increased migratory phenotype, with an enhanced epithelial to mesenchymal transition signature. In summary, our data indicates that DUSP1 and SOX2 have opposite functions in SG-SCC, being DUSP1 necessary for tumor growth and SOX2 dispensable, and with a tumor suppressor function. Our data will suggest that the expression SOX2 and DUSP1 could be a useful biomarker to predict the progression of patients with SG-SCCs.
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Project description:In this dataset, we include the expression data obtained from rat Schwann cells overepressing GFP (control) or Sox2/GFP to identfiy Sox2 tragets in Schwann cells. An in vitro microarray analysis of GFP (control) and Sox2/GFP overexpressing Schwann cells
2018-12-18 | GSE123915 | GEO
Project description:Cancer originates as the progressive accumulation of genetic mutations in proto-oncogenes and tumor suppressors. However, the early events underlying tumor initiation remain largely elusive, mostly due to the general lack of information regarding the cells-of-origin responsible for tumor formation as well as the precise impacts of genetic insults on tumor initiation in vivo. Here, we demonstrate that Sox2-positive (Sox2+) adult stem cells are responsible for epithelial squamous tumor formation. Conditional expression of oncogenic Kras (KrasG12D) and knockout of p53 (also known as Trp53) in Sox2+ cells quickly and specifically resulted in the formation of squamous tumors in the forestomach and esophagus. GFP-based lineage tracing experiments demonstrated that Sox2+ cells are the cells-of-origin of squamous tumors in the esophagus and forestomach. Of note, our data showed that p53 deletion alone did not suffice for tumor initiation. On the contrary, tumor initiation was observed upon KrasG12D activation whereas p53 deletion further contributed to the malignancy of the generated tumors, pointing out distinct roles for Kras activation and p53 deletion in squamous tumor formation and progression, to which a multihit carcinogenesis model can be applied. Global gene expression analysis revealed secreting factors upregulated in the generated tumors induced by oncogenic Kras, which contribute to tumor progression. Taken together, these results demonstrate that epithelial squamous tumors can specifically originate as a consequence of defined genetic mutations in a Sox2+ cell population and highlight the connections between proliferative stem cells and tumor development in vivo.
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Project description:Protein-protein proximity of core pluripotency transcription factors plays an important role during cell reprogramming. Pluripotent embryonic stem (ES) cell identity is controlled by a trio of transcription factors: Sox2, Oct4, and Nanog. These proteins often bind to closely localized genomic sites. The precise mode by which Sox2, Oct4, and Nanog interact with DNA is likely to make a crucial contribution to their function. Here, a detailed protocol for in vivo detection and quantitative analysis of protein-protein proximity of Sox2 and Oct4 using Proximity Utilizing Biotinylation (PUB) method based on the use of the BAP/BirA (target/enzyme) system is described. The method includes design and cloning of DNA plasmid construct, transient transfection of HEK293T cells, Western blot analysis of nuclei fraction and LC-MS/MS analysis. Experiments with coexpression of BAP-X+BirA-Y (X, Y=Sox2, Oct4 and GFP as control) revealed strong biotinylation level of target proteins when X and Y were pluripotency transcription factors compared with control when X=GFP. Since mass spectrometry provides both high sensitivity and more accurate quantification of data a modified workflow was used, in which SDS-PAGE step was eliminated and His-tagged BAP-fused proteins from cell lysate were purified in 6M guanidine HCl buffer, washed, propionylated, digested directly on the Ni sepharose beads using trypsin and analysed on Q-TOF Impact II instrument. Using mass spectrometry allows making quantitative estimation of in vivo interaction of BAP-Sox2 and BirA-Oct4 which was demonstrated by measuring ratios of biotinylation levels of BAP fused either with Sox2 or GFP at different biotin pulse times. After vector preparation this protocol can be completed in seven working days.
2020-01-21 | PXD015756 | Pride
Project description:In this experiment, we identify MYC binding sites in the medulloblastoma cell line ONS76. The purpose of this experiment was to identify genes bound by MYC and compare MYC bound genes to genes differentially expressed when SOX2 or omomyc were elevated in ONS76 cells.
2022-08-22 | GSE186834 | GEO