MiR-1246 was found to promote tumorigenesis and metastasis in sevearl cancer types. In the context of tumor microenvironment, tumor-associated macrophages are a central part typically correlated with poor prognosis.
Mutant p53 cancers reprogram macrophages to tumor supporting macrophages via exosomal miR-1246.
Specimen part
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Comparative expression analysis reveals lineage relationships between human and murine gliomas and a dominance of glial signatures during tumor propagation in vitro.
Sex, Age, Specimen part, Disease stage
View SamplesIn this study, we screened a cohort of 57 paediatric brain tumours, with a wide range of pathologies to identify gene expression profiles
Comparative expression analysis reveals lineage relationships between human and murine gliomas and a dominance of glial signatures during tumor propagation in vitro.
Sex, Age, Specimen part, Disease stage
View SamplesExpression profiling of MRC5, IFN gamma treated MRC5 and PGF cells.
Reconfiguration of genomic anchors upon transcriptional activation of the human major histocompatibility complex.
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View SamplesThe effects of mutant p53 on TNFa stimulated PANC1 cells was tested.
Mutant p53 prolongs NF-κB activation and promotes chronic inflammation and inflammation-associated colorectal cancer.
Specimen part, Cell line
View SamplesCircadian rhythm study on transcriptional responses to i.v. administered 90 kBq iodine-131 after 24h in mouse kidney cortex and medulla, liver, lungs, spleen, and thyroid.
Circadian rhythm influences genome-wide transcriptional responses to (131)I in a tissue-specific manner in mice.
Sex, Specimen part, Time
View SamplesTranscriptomic profiling of normal mouse thyroid tissue following 211At irradiation
Transcriptional response of BALB/c mouse thyroids following in vivo astatine-211 exposure reveals distinct gene expression profiles.
Specimen part
View SamplesRNA microarray analysis of low-dose and dose rate responses versus time after i.v. administration of 211At.
Transcriptional response in normal mouse tissues after i.v. (211)At administration - response related to absorbed dose, dose rate, and time.
Sex, Specimen part, Time
View SamplesBromodomain and extra terminal domain (BET) proteins are important epigenetic regulators facilitating the transcription of genes in chromatin areas linked to acetylated histones. JQ1, a BET protein inhibitor, has antiproliferative activity against many cancers, mainly through inhibition of c-MYC and upregulation of p21. In this research, we investigated the use of JQ1 for human osteosarcoma (OS) treatment. JQ1 significantly inhibited the proliferation and survival of OS cells inducing G1 cell cycle arrest, premature senescence, but little effect on apoptosis. Interestingly, c-MYC protein levels in JQ1-treated cells remained unchanged, whereas the upregulation of p21 protein was still observable. Although effective in vitro, JQ1 alone failed to reduce the size of the MNNG/HOS xenografts in immunocompromised mice. To overcome the resistance of OS cells to JQ1 treatment, we combined JQ1 with rapamycin, an mTOR inhibitor. JQ1 and rapamycin synergistically inhibited the growth and survival of OS cells in vitro and in vivo. We also identified that RUNX2 is a direct target of BRD4 inhibition by JQ1 in OS cells. Chromatin immunoprecipitation (ChIP) showed that enrichment of BRD4 protein around RUNX2 transcription start sites diminished with JQ1 treatment in MNNG/HOS cells. Overexpression of RUNX2 protected JQ1-sensitive OS cells from the effect of JQ1, and siRNA-mediated inhibition of RUNX2 sensitized the same cells to JQ1. In conclusion, our findings suggest that JQ1, in combination with rapamycin, is an effective chemotherapeutic option for OS treatment. We also show that inhibition of RUNX2 expression by JQ1 partly explains antiproliferative activity of JQ1 in OS cells.
Synergistic effect of JQ1 and rapamycin for treatment of human osteosarcoma.
Specimen part, Cell line
View SamplesAnalysis of histone acetyl transferases (HATs) from the MYST and GNAT families in S. pombe to identify functional differences or overlap with regard to gene expression. Mutations were made to Elp3 and Gcn5 (GNAT family), and to Mst2 (MYST family). Mutants showed distinct phenotypes which were repressed or enhanced by mutant combinations.
Expression profiling of S. pombe acetyltransferase mutants identifies redundant pathways of gene regulation.
Cell line, Treatment
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