Expression data from TGFBR3 controls and TGFBR3 knockdown of SUM159 3D cultures
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Moses Harold
PROVIDER: S-ECPF-GEOD-54756 | biostudies-other |
REPOSITORIES: biostudies-other
Similar Datasets
Project description:The objective of this experiment was to determine global gene expression change in triple negative cell line upon knockdown of TGFBR3. Genotype specific differences in expression profiles have been evaluated using human HuGene1.0-ST affymetrix array. RNA was extracted from SUM159 controls and SUM159 TGFBR3KD cells cultured in 3-dimensional in vitro system.
2014-02-06 | GSE54756 | GEO
Project description:The objective of this experiment was to determine global gene expression change in triple negative cell line upon knockdown of TGFBR3. Genotype specific differences in expression profiles have been evaluated using human HuGene1.0-ST affymetrix array. RNA was extracted from SUM159 controls and SUM159 TGFBR3KD cells cultured in 3-dimensional in vitro system. Control (N=3) and TGFBR3KD (N=3) samples were hybridized to the Human gene 1.0 ST array, scanned with Affymetrix using AGCC v. 3.2.4 and then analyzed in R 3.0.1 using the oligo package.
2014-02-06 | E-GEOD-54756 | biostudies-arrayexpress
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Project description:De novo lipogenesis is activated in most cancers. Several lipogenic enzymes are implicated in oncogenesis and represent potential cancer therapeutic targets. RNA interference-mediated depletion of ATP citrate lyase (ACLY), the enzyme that catalyzes the first step of de novo lipogenesis, leads to growth suppression in a subset of human cancer cells. Here we demonstrate the molecular basis and potential biomarkers for ACLY-targeting therapy. First, suppression of cancer cell growth by ACLY depletion involves down-regulation of fatty acid elongase ELOVL6 at the transcriptional level. Lipid profiling revealed that ACLY depletion alters fatty acid composition in triglyceride; increased palmitate and decreased longer fatty acids, in accordance with ELOVL6 down-regulation. Second, ACLY depletion increases reactive oxygen species (ROS), whereas addition of antioxidant reduces ROS and attenuates the growth suppression. Third, ACLY depletion or ROS stimulation induce phosphorylation of AMP-activated protein kinase (AMPK), a sensor of energy and lipid metabolism. Analysis of various cancer cell lines revealed that the levels of AMPK phosphorylation (p-AMPK) correlate with the basal ROS levels, and that cancer cells with low basal p-AMPK (i.e., low basal ROS) levels are highly susceptible to ACLY depletion-mediated growth suppression. Finally, in clinical colon cancer tissues, p-AMPK levels are significantly decreased in aggressive tumors and correlate with the levels of 8-hydroxydeoxyguanosine, a hallmark of ROS stimulation. Together, these data suggest that ACLY inhibition suppresses cancer growth via palmitate-mediated lipotoxicity, and p-AMPK could be a predictive biomarker for its therapeutic outcome. Two cell lines are treated with ACLY siRNA. The samples include controls of each cell line.
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Project description:In our lab we detected focal genomic amplification of PDE1C in 90% of short term GBM cultures. Knocking down of PDE1C was associated with compromised capacity opf these cultures to proliferate, migrate and invade. Therefore we carried out affymetric whole genome expression analysis to identify the down stream gene effectors of this function effects.
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Project description:miR-21 is overexpressed in breast cancer cells. Knock-down of miR-21 cause apoptosis and decreased cell proliferation. To identify miR-21 regulated cancer-pathways in MCF-7 cells, we knocked-down miR-21 and performed microarray. RNA was harvested from MCF-7 cells 24 hours transfection of anti-control, anti-21, or untreated cells. RNA was processed and hybridized into Affymetrix whole human genome arrays in duplicates.
| S-ECPF-GEOD-52674 | biostudies-other
Project description:In our lab we detected focal genomic amplification of PDE1C in 90% of short term GBM cultures. Knocking down of PDE1C was associated with compromised capacity opf these cultures to proliferate, migrate and invade. Therefore we carried out affymetric whole genome expression analysis to identify the down stream gene effectors of this function effects. IN1472 and IN1760 - 2 GBM short term cultures were transfected with siRNA either for PDE1C (siPD) or non-targeting (siNT) and its down gene effectors were studied.
2013-05-02 | E-GEOD-46538 | biostudies-arrayexpress