Expression data from SSEA1+ c-kit+ differentiated murine embryonic stem cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Anne Lindgren
PROVIDER: E-GEOD-25465 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:SSEA1+ cells sorted from mouse embryonic stem cells differentiated for 4 days in 10uM Retinoic acid do not form teratomas when transplated into SCID mice while Pten-/- cells do. We used microarrays to identify genes and pathways besides Pten that could explain this difference in tumorigenicity. Keywords: wild type vs Pten-/- Wild type and Pten mutant SSEA1 positive differentiated cells were compared as the wild type cells were non-tumorigenic upon transplant to SCID mice and the Pten-/- cells were tumorigenic.
2010-09-11 | E-GEOD-24078 | biostudies-arrayexpress
Project description:SSEA1+ cells sorted from mouse embryonic stem cells differentiated for 4 days in 10uM Retinoic acid do not form teratomas when transplated into SCID mice while Pten-/- cells do. We used microarrays to identify genes and pathways besides Pten that could explain this difference in tumorigenicity. Keywords: wild type vs Pten-/-
2010-09-11 | GSE24078 | GEO
Project description:SSEA1+ c-kit+cells sorted from mouse embryonic stem cells differentiated for 4 days in 10uM Retinoic acid do not form teratomas when transplated into SCID mice while Pten-/- cells do. We used microarrays to identify genes and pathways besides Pten that could explain this difference in tumorigenicity.
2010-11-19 | GSE25465 | GEO
Project description:We used microarrays to identify the gene expression changes in Cbx1-/- (HP1beta) knockout embryonic stem cells (ESCs) and Cbx5-/- (HP1alpha) knockout ESCs compared to WT ESCs and in embryoid bodies (EBs) differentiated from those three ESC types. ESCs were grown and the pluripotent SSEA1-positive cells from all ESC types using MACS were sorted and harvested or sorted and differentiated into EBs. Total RNA from all samples was extracted.
2015-08-02 | E-GEOD-65121 | biostudies-arrayexpress
Project description:Prostate cancer is the most commonly diagnosed and second-most lethal cancer among men in the United States. The vast majority of prostate cancer deaths are due to castration-resistant prostate cancer (CRPC) â?? the lethal form of the disease that has progressed despite therapies that interfere with activation of androgen receptor (AR) signaling. One emergent resistance mechanism to medical castration is synthesis of intratumoral androgens that activate the AR. This insight led to the development of the AR antagonist enzalutamide. However, resistance to enzalutamide invariably develops, and disease progression is nearly universal. One mechanism of resistance to enzalutamide is an F877L mutation in the AR ligand-binding domain that can convert enzalutamide to an agonist of AR activity. However, mechanisms that contribute to the agonist switch had not been fully clarified, and there were no therapies to block AR F877L. Using cell line models of castration-resistant prostate cancer (CRPC), we determined that cellular androgen content influences enzalutamide agonism of mutant F877L AR. Further, enzalutamide treatment of AR F877L-expressing cell lines recapitulated the effects of androgen activation of F877L AR or wild-type AR. Because the BET bromodomain inhibitor JQ-1 was previously shown to block androgen activation of wild-type AR, we tested JQ-1 in AR F877L-expressing CRPC models. We determined that JQ-1 suppressed androgen or enzalutamide activation of mutant F877L AR and suppressed growth of mutant F877L AR CRPC tumors in vivo, demonstrating a new strategy to treat tumors harboring this mutation. RNA-seq profiles of prostate cancer cell lines to understand gene expression associated with enzalutamide treatment
2016-06-10 | E-GEOD-69896 | biostudies-arrayexpress
Project description:Tbx3, a member of the T-box family, plays important roles in development, stem cells, nuclear reprogramming and cancer. Loss of Tbx3 induces differentiation in mouse embryonic stem cells (mESCs). However, we show that mESCs exist in an alternate stable pluripotent state in the absence of Tbx3. In-depth transcriptome analysis of this mESC state reveals Dppa3 as a direct downstream target of Tbx3. Also Tbx3 facilitates the cell fate transition from pluripotent cells to mesoderm progenitors by directly repressing Wnt pathway members required for differentiation. Wnt signaling regulates differentiation of mESCs into mesoderm progenitors and helps maintain a naïve pluripotent state. We show that Tbx3, a downstream target of Wnt signaling, fine-tunes these divergent roles of Wnt signaling in mESCs. In conclusion, we identify a signaling-TF axis that controls the exit of mESCs from a self-renewing pluripotent state towards mesoderm differentiation. ChIPSeq and RNASeq (population and single cell) was performed on the indicated cell lines. Replicates are indicated as needed. The mm9 genome assembly was used. For single cell mRNA-Seq preparation, SSEA1+DAPI- mESCs were sorted and collected.
2015-07-21 | E-GEOD-60066 | biostudies-arrayexpress
Project description:Nodal and Activin are morphogens of the TGFbeta superfamily of signaling molecules that direct differential cell fate decisions in a dose- and distance-dependent manner. During early embryonic development the Nodal/Activin pathway is responsible for the specification of mesoderm, endoderm, node and mesendoderm. In contradiction to this drive towards cellular differentiation, the pathway also plays important roles in the maintenance of self-renewal and pluripotency in embryonic and epiblast stem cells. The molecular basis behind stem cell interpretation of Nodal/Activin signaling gradients and the undertaking of disparate cell fate decisions remains poorly understood. Here, we show that any perturbation of endogenous signaling levels in mouse ES cells leads to their exit from self renewal towards divergent differentiation programs. Increasing Nodal signals above basal levels by direct stimulation with Activin promotes differentiation towards the mesendodermal lineages while repression of signaling with the specific Nodal/Activin receptor inhibitor SB431542 induces trophectodermal differentiation. To address how quantitative Nodal/Activin signals are translated qualitatively into distinct cell fates decisions, we performed chromatin immunoprecipitation of phospho-Smad2 the primary downstream transcriptional factor of the Nodal/Activin pathway followed by massively parallel sequencing and show that phospho-Smad2 binds to and regulates distinct subsets of target genes in a dose-dependent manner. Crucially, Nodal/Activin signaling directly controls the Oct4 master regulator of pluripotency by graded phospho-Smad2 binding in the promoter region. Hence stem cells interpret and carry out differential Nodal/Activin signaling instructions via a corresponding gradient of Smad2 phosphorylation that selectively titrates self-renewal against alternative differentiation programs by direct regulation of distinct target gene subsets and Oct4 expression. Four biological replicates consisting of 4 different passages of E14TG2a ES cells at P20, P21, P23 and P24
2011-06-30 | E-GEOD-23239 | biostudies-arrayexpress
Project description:Salts of aluminium, a chemical element devoid of biological function, are added to many industrial products of frequent use because of aluminium's chemical versatility. As a result of lifetime exposure, aluminium accumulates in several organs including the mammary gland. At concentrations in the range of those measured in the breast of women living in industrialised countries, aluminium chloride transforms human and mouse mammary epithelial cells in vitro. These results challenge the safety commonly ascribed to aluminium and suggest that it could be a human carcinogen. HC11 is a spontaneously immortalised, non tumorigenic mouse mammary epithelial cell line originally derived from Balb/c mice that, following chronic culture in the presence of aluminium - in the form of AlCl3 x 6H2O - becomes able to form tumors and metastasis in the immunocompetent and immunocompatible strain Balb/cByJ. As a part of our investigations on the mechanisms by which aluminium might transform mammary epithelial cells, we analysed the mRNA profile of HC11 cells transformed in vitro by aluminium or the corresponding untreated controls cultured in parallel by cDNA microarray. We used the Clariom S microarray from Thermofisher, that covers more than 20'000 well annotated mRNAs.
2020-11-30 | E-MTAB-9723 | biostudies-arrayexpress
Project description:The estrogen-dependence of breast cancer has long been recognized, however, the role of 17β-estradiol (E2) in cancer initiation was not known until we demonstrated that it induces complete neoplastic transformation of the human breast epithelial cells MCF-10F. E2-treatment of MCF-10F cells progressively induced high colony efficiency and loss of ductulogenesis in early transformed (trMCF) cells and invasiveness in Matrigel invasion chambers. The cells that; crossed the chamber membrane were collected and identified as bsMCF, and their subclones designated bcMCF, and the cells harvested from carcinoma formation in SCID mice designated caMCF. These phenotypes correlated with gene dysregulation during the progression of the ; transformation. The highest number of dysregulated genes was observed in caMCF, being slightly lower in bcMCF, and lowest in trMCF. This order was consistent with the extent of chromosome aberrations (caMCF > bcMCF >>> trMCF). Chromosomal amplifications were found in 1p36.12-pter, 5q21.1-qter and 13q21.31-qter. Losses of the complete chromosome 4 and 8p11.21-23.1 were found only in tumorigenic cells. In tumor-derived cell lines, additional losses were found in 3p12.1-14.1, 9p22.1-pter and 18q11.21-qter. Functional profiling of dysregulated genes revealed progressive changes in the integrin signaling pathway, inhibition of apoptosis, acquisition of tumorigenic cell surface markers and epithelial-mesenchymal transition. In tumorigenic cells, the levels of E-cadherin, EMA, and various keratins were low and CD44E/CD24 were negative, whereas SNAI2, vimentin, S100A4, FN1, HRAS, TGFβ1 and; CD44H were high. The phenotypic and genomic changes triggered by estrogen exposure that lead normal cells to tumorigenesis confirm the role of this steroid hormone in cancer initiation. Experiment Overall Design: Human MCF-10F cells were transformed by 70nM 17-beta-estradiol. The transformed cells were selected by Boyden chamber. The selected cells were injected into SCID mice and also cloned and expanded. The thus grown tumors were harvested for cell culture. Genomic DNA and total RNA were isolated from cell lines in each step for 100K SNP and gene expression microarray assay.
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