Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1070015 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27749300_1.fastq.gz | Fastqsanger.gz | |||
| SRR27749300_2.fastq.gz | Fastqsanger.gz | |||
| SRR27749301_1.fastq.gz | Fastqsanger.gz | |||
| SRR27749301_2.fastq.gz | Fastqsanger.gz | |||
| SRR27749278_1.fastq.gz | Fastqsanger.gz |
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Project description:Nontransformed cells form heterotypic cadherin junctions with adjacent transformed cells to inhibit tumor cell growth and motility. Transformed cells must override this form of growth control, called contact normalization, to invade and metastasize during cancer progression. Heterocellular cadherin junctions between transformed and nontransformed cells are needed for this process. However, specific mechanisms downstream of cadherin signaling have not been clearly elucidated. Here, we utilized a b-catenin reporter construct to determine if contact normalization affects Wnt signaling in transformed cells. b-catenin driven GFP expression in Src transformed mouse embryonic cells was decreased when cultured with cadherin competent nontransformed cells compared to transformed cells cultured with themselves, but not when cultured with cadherin deficient nontransformed cells. We also utilized a layered culture system to investigate the effects of oncogenic transformation and contact normalization on gene expression and oncogenic Src kinase mediated phosphorylation events. RNA-Seq analysis found that the cadherin dependent contact normalization inhibited the expression of 22 transcripts that were induced by Src transformation, and increased the expression of 78 transcripts that were suppressed by Src transformation. Phosphoproteomic analysis of cells expressing a temperature sensitive Src kinase construct found that contact normalization decreased phosphorylation of 10 proteins on tyrosine residues that were phosphorylated within 1 hour of Src kinase activation in transformed cells. Taken together, these results indicate that cadherin dependent contact normalization inhibits Wnt signaling to regulate oncogenic kinase activity and gene expression, particularly PDPN expression, in transformed cells in order to control tumor progression.
2024-02-19 | MSV000094121 | MassIVE
Project description:To address the molecular mechanisms underlying c-Src-mediated tumor progression, we previously developed a model system using Csk-deficient fibroblasts that can be transformed by wild-type c-Src. In this study, we applied this system for the analysis of the potential contribution of miRNA to c-Src-mediated transformation. Pair-wise significance analysis of the microarray indicated that seven miR genes were significantly upregulated and six miRNA genes were downregulated in c-Src-transformed cells with a P value below 0.01 and with a fold change over 2.0.
2011-02-17 | GSE23426 | GEO
Project description:We reported that stable expression of constitutively active intra cellular Notch (ICN), in quail neuroretina (QNR) cells transformed by a conditional v-Src mutant (QNR/v-src cells), resulted in the suppression of their transformed properties. Acquisition of a normal phenotype coincided with a major switch in cell identity, as these undifferentiated QNR/v-src cells acquired characteristics of glial differentiation. Similar loss of transformation and gene reprogramming can be achieved in QNR/v-src cells, stably expressing the human CBF protein, RBP-Jk, whose activity was rendered ligand independent by fusion to the VP16 transactivator. These major phenotypic changed are correlated with a dominant interference with signaling effectors, regulating cell morphology and cytoskeleton organization. To understand the mechanisms by which Notch signaling activation suppressed v-Src induced cell transformation and induced differentiation, we compared the transcription profile of QNR cells transformed by a v-Src mutant encoding a temperature sensitive oncoprotein (QNR/v-src), with that of cells stably expressing ICN (QNR/v-src/ICN) or RBP-Jk-VP16 (QNR/v-src/RBP-Jk-VP16).
2010-12-01 | GSE22054 | GEO
Project description:We reported that stable expression of constitutively active intra cellular Notch (ICN), in quail neuroretina (QNR) cells transformed by a conditional v-Src mutant (QNR/v-src cells), resulted in the suppression of their transformed properties. Acquisition of a normal phenotype coincided with a major switch in cell identity, as these undifferentiated QNR/v-src cells acquired characteristics of glial differentiation. Similar loss of transformation and gene reprogramming can be achieved in QNR/v-src cells, stably expressing the human CBF protein, RBP-Jk, whose activity was rendered ligand independent by fusion to the VP16 transactivator. These major phenotypic changed are correlated with a dominant interference with signaling effectors, regulating cell morphology and cytoskeleton organization. To understand the mechanisms by which Notch signaling activation suppressed v-Src induced cell transformation and induced differentiation, we compared the transcription profile of QNR cells transformed by a v-Src mutant encoding a temperature sensitive oncoprotein (QNR/v-src), with that of cells stably expressing ICN (QNR/v-src/ICN) or RBP-Jk-VP16 (QNR/v-src/RBP-Jk-VP16). Total RNA was extracted from QNR/v-src, QNR/v-src/ICN or QNR/v-src/RBP-Jk-VP16 cells maintained at permissive (37°C) or restrictive (41°C) temperature. cDNA from QNR/v-src cells was probed with that of QNR/v-src/ICN or QNR/v-src/RBP-Jk-VP16 at both temperature on microarrays spotted with 13,000 cDNA from chicken EST collections designed by the genomic facility of the Fred Hutchinson Cancer Research Center (Seattle). For two sets of sample, dye swap experiments were performed.
2010-12-01 | E-GEOD-22054 | biostudies-arrayexpress
Project description:Gene profiling of v-Src transformed primary chicken cells
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Project description:Primary prostate epithelial cell cultures were established from the VENTRAL prostates of FVB mice . Cells were transduced with retroviral expression vectors encoding a single distinct oncogene (c-Myc, Ha-Ras (V-12), v-Src and NeuT, an activating mutant of ErbB2). Individual colonies of oncogene-transduced cells were selected and characterized. These cell lines demonstrate contact-independent growth characteristics in soft agar and in immune competent mice. To further characterize the molecular genetic signaling pathways regulated by specific oncogenes in prostate epithelial cells mRNA was prepared from the oncogene transformed PEC cell lines, 12 samples(each oncogene has 3 lines) and 3 normal prostate epithelial cell controls in good condition.
2013-04-01 | E-GEOD-37428 | biostudies-arrayexpress
Project description:Tumor invasion into surrounding stromal tissue is a hallmark of high-grade, metastatic cancers. Oncogenic transformation of human epithelial cells in culture can be triggered by activation of v-Src kinase, resulting in increased cell motility, invasiveness and tumorigenicity and provides a valuable model for studying how changes in gene expression cause cancer phenotypes. Here, we show that epithelial cells transformed by activated Src show increased levels of DNA methylation and that the methylation inhibitor, 5-AzaC, potently blocks the increased cell motility and invasiveness induced by Src activation. A proteomic screen for chromatin regulators acting downstream of activated Src identified the replication-dependent histone chaperone CAF1 as an important factor for Src-mediated increased cell motility and invasion. We show Src causes a 5-AzaC-sensitive decrease in both mRNA and protein levels of the p150 (CHAF1A) and p60 (CHAF1B), subunits of CAF1. Depletion of CAF1 in untransformed epithelial cells using siRNA was sufficient to recapitulate the increased motility and invasive phenotypes characteristic of transformed cells without activation of Src. Maintaining high levels of CAF1 by exogenous expression suppressed the increased cell motility and invasiveness phenotypes when Src was activated. These data identify a critical role of CAF1 in the dysregulation of cell invasion and motility phenotypes seen in transformed cells and also highlight an important role for epigenetic remodeling through DNA methylation for Src-mediated induction of cancer phenotypes.
2016-12-20 | PXD005494 | Pride
Project description:To address the molecular mechanisms underlying c-Src-mediated tumor progression, we previously developed a model system using Csk-deficient fibroblasts that can be transformed by wild-type c-Src. In this study, we applied this system for the analysis of the potential contribution of miRNA to c-Src-mediated transformation. Pair-wise significance analysis of the microarray indicated that seven miR genes were significantly upregulated and six miRNA genes were downregulated in c-Src-transformed cells with a P value below 0.01 and with a fold change over 2.0. Csk-/- mouse embryonic fibroblasts (Csk-/- MEFs) were transfected with empty vector, c-Src, Csk/c-Src, or Csk. Each sample was run in duplicate.
2011-02-17 | E-GEOD-23426 | biostudies-arrayexpress
Project description:To address the molecular mechanisms underlying c-Src-induced cell transformation, we previously developed a model system using Csk-deficient fibroblasts that can be transformed by wild-type c-Src. In this study, we applied this system for the analysis of the potential contribution of mRNA and miRNA to c-Src-induced cell transformation. We found miR-129-3p was downregulated in c-Src-induced cell transformation in a Dox-inducible expression system via c-Src, c-Yes, and Fer.
2019-12-08 | GSE121853 | GEO
Project description:Long non-coding RNAs (lncRNAs) have been implicated in normal cellular homeostasis as well as pathophysiological conditions, including cancer. Here we performed global gene expression profiling of mammary epithelial cells transformed by oncogenic v-Src, and identified a large subset of uncharacterized lncRNAs potentially involved in breast cancer development. Specifically, our analysis revealed a novel lncRNA, LINC00520 that is upregulated upon ectopic expression of oncogenic v-Src, in a manner that is dependent on the transcription factor STAT3. Similarly, LINC00520 is also increased in mammary epithelial cells transformed by oncogenic PI3K and its expression is decreased upon knockdown of mutant PIK3CA. Additional expression profiling highlight that LINC00520 is elevated in a subset of human breast carcinomas, with preferential enrichment in the basal-like molecular subtype. ShRNA-mediated depletion of LINC00520 results in decreased cell migration and loss of invasive structures in 3D. RNA sequencing analysis uncovers several genes that are differentially expressed upon ectopic expression of LINC00520, a significant subset of which are also induced in v-Src-transformed MCF10A cells. Together, these findings characterize LINC00520 as a lncRNA that is regulated by oncogenic Src, PIK3CA and STAT3, and which may contribute to the molecular etiology of breast cancer.
2016-08-30 | GSE86159 | GEO