Reactive oxygen species (ROS) are implicated in tumor transformation by modulating proteins involved in differentiation, proliferation and invasion. In order to identify genes that may support melanoma progression or regression after an antioxidant system (AOS) response, we developed and characterized a human melanoma cell model with different levels of ROS by stably overexpressing the antioxidant enzyme catalase in A375 amelanotic melanoma cells, and whole genome gene expression patterns were analyzed by microarrays.
Reprogramming human A375 amelanotic melanoma cells by catalase overexpression: Upregulation of antioxidant genes correlates with regression of melanoma malignancy and with malignant progression when downregulated.
Specimen part, Cell line
View SamplesThe mRNA processing body is a cellular structure that regulates the stability of cytoplasmic mRNA. MARF1/LMKB is an RNA-binding protein that is associated with maintenance of mRNA homeostasis and genomic stability. To investigate the function of LMKB in a human B lymphocyte cell line, BJAB cells were treated with either control lentivirus or a lentivirus containing LMKB siRNA.
LMKB/MARF1 localizes to mRNA processing bodies, interacts with Ge-1, and regulates IFI44L gene expression.
Specimen part, Cell line
View SamplesWe used microarrays to analyze the global expression patterns for 22 commercially available pancreatic cancer cell lines
Glycogene expression alterations associated with pancreatic cancer epithelial-mesenchymal transition in complementary model systems.
Specimen part, Cell line
View SamplesTo characterize the transcriptome of the transcription factor AP4 DLD-1 cells were infected with AP4 coding viruses for different periods of time. Adenovirus amplification and purification was performed as previously described (He et al., 1998). The minimal amount of virus needed to reach more than 90% infection efficiency was determined by monitoring GFP signals with fluorescence microscopy. DLD-1 cells were infected in serum-free medium with adenovirus for 3 hours. After removal an equal amount of medium containing 20% FBS was added.
AP4 is a mediator of epithelial-mesenchymal transition and metastasis in colorectal cancer.
Cell line, Time
View SamplesGoal of this experiment is the identify differentially expressed genes in GBM zenografts that have been exposed to Cilengitide for 1 or 8 hours. A control with no cilengitide is also included. None of the tumors recieved radiation.
Radiation sensitization of glioblastoma by cilengitide has unanticipated schedule-dependency.
No sample metadata fields
View SamplesTGF-beta treatment of Panc-1 pancreatic adenocarcinoma cell line on Affymetrix HG_U133_plus_2 arrays; triplicate experiments.
Glycogene expression alterations associated with pancreatic cancer epithelial-mesenchymal transition in complementary model systems.
Specimen part, Cell line, Treatment
View SamplesAcquired drug resistance prevents targeted cancer therapy from achieving stable and complete responses. Emerging evidence implicates a key role for nonmutational mechanisms including changes in cell state during early stages of acquired drug resistance. Targeting nonmutational resistance may therefore present a therapeutic opportunity to eliminate residual surviving tumor cells and impede relapse. A variety of cancer cell lines harbor quiescent, reversibly drug-tolerant “persister” cells which survive cytotoxic drugs including targeted therapies and chemotherapies. These persister cells survive drug through nonmutational mechanisms which are poorly understood. Specifically targeting persister cells is a promising strategy to prevent tumor relapse. We sought to identify therapeutically exploitable vulnerabilities in persister cells using the HER2-amplified breast cancer line BT474 as an experimental model. Similar to other persister cell models, upon treatment with the HER2 inhibitor lapatinib (2uM concentration) for nine or more days, the majority of BT474 cells die, revealing a small population of quiescent surviving persister cells. Removal of lapatinib allows the persister cells to regrow and to re-acquire sensitivity to lapatinib. Subsequent lapatinib treatment re-derives persister cells. The reversibility of persister cell drug resistance indicates a nonmutational resistance mechanism. Here we provide RNAseq gene expression profiling data generated from parental BT474 cells compared to BT474 persister cells generated from nine days of treatment with 2 uM lapatinib. These data can be used to identify genes and pathways which are upregulated in persister cells, revealing potential therapeutic targets. Overall design: 3 biological replicates of BT474 persister cells, two biological replicates of BT474 parental cells
Drug-tolerant persister cancer cells are vulnerable to GPX4 inhibition.
Specimen part, Cell line, Subject
View SamplesWe have used microarray technology to identify the transcriptional targets of Rho subfamily GTPases. This analysis indicated that murine fibroblasts transformed by these proteins show similar transcriptomal profiles. Functional annotation of the regulated genes indicate that Rho subfamily GTPases target a wide spectrum of biological functions, although loci encoding proteins linked to proliferation and DNA synthesis/transcription are up-regulated preferentially. Rho proteins promote four main networks of interacting proteins nucleated around E2F, c-Jun, c-Myc, and p53. Of those, E2F, c-Jun and c-Myc are essential for the maintenance of cell transformation. Inhibition of Rock, one of the main Rho GTPase targets, leads to small changes in the transcriptome of Rho-transformed cells. Rock inhibition decreases c-myc gene expression without affecting the E2F and c-Jun pathways. Loss-of-function studies demonstrate that c-Myc is important for the blockage of cell-contact inhibition rather than for promoting the proliferation of Rho-transformed cells. However, c-Myc overexpression does not bypass the inhibition of cell transformation induced by Rock blockage, indicating that c-Myc is essential, but not sufficient, for Rock-dependent transformation. These results reveal the complexity of the genetic program orchestrated by the Rho subfamily and pinpoint protein networks that mediate different aspects of the malignant phenotype of Rho-transformed cells
Transcriptomal profiling of the cellular transformation induced by Rho subfamily GTPases.
No sample metadata fields
View SamplesVolatiles of certain rhizobacteria can cause growth inhibitory effects on plants/ Arabidopsis thaliana. How these effects are initiated and which mechanisms are enrolled is not yet understood. Obviously the plant can survive/live with the bacteria in the soil, which suggest the existance of a regulatory mechanism/network that provide the possibility for coexistance with the bacteria. To shed light on this regulatory mechanism/network we performed a microarray anlaysis of Arabidopsis thaliana co-cultivated with two different rhizobacteria strains.
Volatiles of two growth-inhibiting rhizobacteria commonly engage AtWRKY18 function.
Age, Specimen part, Time
View SamplesBackground: Studies in mice have shown that PPAR is an important regulator of lipid metabolism in liver and a key transcription factor involved in the adaptive response to fasting. However, much less is known about the role of PPAR in human liver. Here we set out to study the function of PPAR in human liver via analysis of whole genome gene regulation in human liver slices treated with the PPAR agonist Wy14643.
The impact of PPARα activation on whole genome gene expression in human precision cut liver slices.
Sex, Specimen part, Treatment, Subject, Time
View Samples