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Irradiation of healthy brain alters expression of genes involved in cell motility and invasiveness of glioblastoma

ABSTRACT: Irradiation of healthy brain alters expression of genes involved in cell motility and invasiveness of glioblastoma

PROVIDER: PRJNA556205 | ENA |

REPOSITORIES: ENA

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Irradiation of healthy brain alters expression of genes involved in cell motility and invasiveness of glioblastoma

Project description:Traumatic brain injury is known to cause proliferation and migration of astrocytic and neuronal cells. To find out whether irradiation may influence migration of intracranial tumors, we performed expression profiling of orthotopically implanted glioblastomas following irradiation to the contralateral (non-diseased) hemisphere. Microarrays were used to identify differentially expressed genes associated with glioblastoma-malignancy in distinct tumor compartments following irradiation of brain tissue of contralateral (non-diseased) hemisphere. Differentially expressed genes were the object to functional network analysis with Ingenuity pathway analysis software

2020-10-14 | GSE134711 | GEO

Human Schlafen 5 (SLFN5) is a Regulator of Motility and Invasiveness of Renal Cell Carcinoma (RCC) Cells

Project description:There is some emerging evidence that members of the Schlafen (SLFN) family of proteins mediate antineoplastic responses, but the mechanisms accounting for these effects are not known. We provide evidence that human SLFN5, an interferon (IFN)- inducible member of the family, exhibits key roles in controlling motility and invasiveness of renal cell carcinoma (RCC) cells. Our studies define the mechanism by which this occurs, demonstrating that SLFN5 negatively controls expression of matrix metalloproteinases (MMP)-1 and -13 and several other genes involved in the control of malignant cell motility. Importantly, our data establish that SLFN5 expression correlates with a better overall survival in a large cohort of patients with RCC. The inverse relationship between SLFN5 expression and RCC aggressiveness raises the possibility of developing unique therapeutic approaches in the treatment of RCC, by modulating SLFN5 expression.

2015-06-01 | GSE64399 | GEO

The HIF1α/JMY pathway promotes glioblastoma stem-like cell invasiveness after irradiation.

Project description: Not available

| S-EPMC7603339 | biostudies-literature

The chromatin assembly factor complex 1 (CAF1) and 5-Azacytidine (5-AzaC) affect cell motility in Src-transformed human epithelial cells

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

mRNA expression signatures of human glioblastoma stem cell like cells after treatment with FG-3019, irradiation and FG-3019 + irradiation

Project description:To investigate effects on mRNA expression through treatment with FG-3019, irradiation and their combination to gain mechanistic hypotheses on the effects of these treatments on glioblastoma stem cell like cells which have been observed in vitro and in vivo. mRNA expression was measured 6 h after treatment with FG-3019, irradiation and their combination. 3 biological replicates were analyzed for each treatment condition (control, FG-3019, irratiation and FG-3019+irradiation)

2014-08-30 | E-GEOD-60921 | biostudies-arrayexpress

CHD7 promotes glioblastoma cell motility and invasiveness through transcriptional modulation of an invasion signature.

Project description: Not available

| S-EPMC6408455 | biostudies-literature

Gene differential expressions between cell subpopulations with high invasiveness (invaded) and low invasiveness (non-invaded) in human lung cancer H460 cell line

Project description:Cell populations with different invasiveness were isolated and collected with cell culture inserts of Boyden-type cell invasion chambers coated with 1xBME (base membrane extract). Cells that invaded to bottom chamber were collected as cell population with high-invasiveness , and cells that remained in the insert chamber were collected as cell population with low-invasiveness. The selection with Boyden-type cell invasion chambers was repeated six times, and cells with high invasiveness were terms as H-INV subline, and cells with low invasiveness were termed as L-INV subline. Microarray analysis was performed with Illumina HumanHT-12 v4 Expression BeadChips

2015-07-15 | GSE68916 | GEO

Low Dose Gamma Irradiation of Trypanosoma evansi Parasites Identifies Gene Transcripts Involved in Establishing Disease in Mice Post Irradiation

Project description:Transcriptome analysis of irradiated T evansi parasites The protozoan parasite Trypanosoma evansi is responsible for causing Surra in a variety of mammalian hosts over a wide geographical area. In order to identify which genes and processes are required to establish disease in mice, parasites were irradiated over a range using a Cobalt60 gamma source. A custom Trypanosome spp. array that covers the genomes of three trypanosome species, T. brucei, T. evansi and T. congolense was designed by Affymetrix with an average of 9300 whole gene transcripts from all three species were targeted. Irradiation differentially affected the abundance of gene transcripts in a dose-dependent trend. We present these genes as necessary for repair from irradiation damage, and essential for disease establishment in mice post irradiation.

2023-05-06 | GSE202334 | GEO

Histone deacetylase inhibitors impair glioblastoma cell motility and proliferation

Project description:Histone deacetylase inhibitors impair glioblastoma cell motility and proliferation

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Intestinal ablation of CKIalpha highlights invasiveness control

Project description:Wnt signaling, which drives the rapid self-renewal of the gut epithelium is causally associated with intestinal neoplasia. Here we show that CKIalpha is a activation depends on p53 and p21Waf1/Cip1: CKIα ablation provokes activation of p53 and p21, which assume a pivotal role in suppressing invasive cancer. Dual loss of CKIalpha and either p53 or p21 results in rapid, rampant malignant signature denoted p53supinv (p53-suppressed invasiveness) that is conditionally induction of invasiveness. Like invasiveness control, the transcriptional suppression of p53supinv genes is largely mediated by p21, independently of cell cycle control, representing a novel tumor suppressor function of wild-type p53.

2010-10-23 | GSE24760 | GEO

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