Analysis of synchronized HCT116 cells at various time points up to 10 hours following treatment with DMSO or Nocodazole.
A signature-based method for indexing cell cycle phase distribution from microarray profiles.
Cell line, Treatment
View SamplesUsing Affymetrix HG-U133-Plus 2.0 array and Laser Capture Microdissection techniques, we determined whether growth in different zones of the same tumor affected expression of genes by human pancreatic cancer cells. Human L3.6pl pancreatic cancer cells were implanted into the pancreas of nude mice. Gene expression patterns in tumor cells within the central and peripheral zones were compared and statistical differences were determined for 1222 genes. Bioinformatic functional prediction analysis revealed that 346 upregulated genes in the peripheral zone were related to cytoskeleton organization and biogenesis, cell cycle, cell adhesion, cell motility, DNA replication, localization, integrin-mediated signaling pathway, development, morphogenesis, and IkB kinase/NF-kB cascade; and 876 upregulated genes in the central zone were related with regulation of cell proliferation, regulation of transcription, transmembrane receptor protein tyrosine kinase signaling pathway, response to stress, small GTPase mediated signal transduction, hexose metabolism, cell death, response to external stimulus, carbohydrate metabolism, and response to wounding. Results from the microarray were confirmed for reliability by in situ hybridization analysis. Collectively, these data demonstrate zonal heterogeneity for gene expression profiles in tumors and suggest that characterization of zonal gene expression profiles are essential to obtain reproducible data, to predict disease prognosis, and to design specific therapeutics.
Zonal heterogeneity for gene expression in human pancreatic carcinoma.
No sample metadata fields
View Samples17beta-hydroxysteroid dehydrogenase type12 (HSD17B12) has been demonstrated to be involved in regulation of in situ biosynthesis of estradiol (E2). HSD17B12 expression was reported in breast carcinomas but its functions have remained unknown. Therefore, we examined the correlation between mRNA expression profiles determined by microarray analysis and tissue E2 concentrations obtained from 16 postmenopausal breast carcinoma cases in order to analyze an association of the enzyme expression with intratumoral E2 production. No significant correlations were detected between intratumoral HSD17B12expression and E2 concentration.These findings suggest that the presence of HSD17B12 in carcinoma cells contributes to a development of human breast carcinoma via a pathway other than in situ E2 biosynthesis.
17Beta-hydroxysteroid dehydrogenase type 12 in human breast carcinoma: a prognostic factor via potential regulation of fatty acid synthesis.
Sex, Specimen part
View SamplesWe previously identified TLR-independent expression of 4933430F08Rik, encoding Batf2, in T. cruzi-infected bone marrow-derived dendritic cells (BMDCs) (Kayama et al., 2009). To determine the functions of Batf2 in innate immune responses, we performed a comprehensive gene expression analysis in wild-type and Batf2-/- bone marrow-derived macrophages (BMMf). RNA-seq analysis showed that 98 genes are upregulated in Batf2-/- BMMf stimulated with LPS following IFN-? treatment, when compared with that in wild-type cells. Among these genes, we focused on Il23a, encoding IL-23p19, because IL-23 is able to promote expression of Il17a in Th17 cells. Overall design: mRNA of wild-type and Batf2-/- BMMf were subjected to deep sequencing profiling using Illumina HiSeq 2000.
BATF2 inhibits immunopathological Th17 responses by suppressing <i>Il23a</i> expression during <i>Trypanosoma cruzi</i> infection.
Specimen part, Treatment, Subject, Time
View SamplesNIH3T3 in the middle of G0 to G1 transion consists of the cells which is still staying G0 phase and the cells which enters G1. Monitoring the expressions of p27 and Cdt1 enables to distinguish these two; p27+/Cdt1+ cells as the cells in G0 phase and p27-Cdt1+ cells as G1 phase
A novel cell-cycle-indicator, mVenus-p27K-, identifies quiescent cells and visualizes G0-G1 transition.
Cell line
View SamplesDetermine the effect and specificity of HDAC2 siRNA compared to SAHA inhibition of HDAC2 in hepatocellular carcinoma (HCC)
Antitumor effects in hepatocarcinoma of isoform-selective inhibition of HDAC2.
Cell line, Treatment
View SamplesMutations in TGFBR2, a component of the transforming growth factor (TGF)- signaling pathway, occur in high-frequency microsatellite instability (MSI-H) colorectal cancer (CRC). In mouse models, Tgfbr2 inactivation in the intestinal epithelium accelerates the development of malignant intestinal tumors in combination with disruption of the Wnt--catenin pathway. However, no studies have further identified the genes influenced by TGFBR2 inactivation following disruption of the Wnt--catenin pathway. We previously described CDX2P-G19Cre;Apcflox/flox mice, which is stochastically null for Apc in the colon epithelium. In this study, we generated CDX2P-G19Cre;Apcflox/flox;Tgfbr2flox/flox mice, with simultaneous loss of Apc and Tgfbr2. These mice developed tumors, including adenocarcinoma in the proximal colon. We compared gene expression profiles between tumors of the two types of mice using microarray analysis.
Gasdermin C Is Upregulated by Inactivation of Transforming Growth Factor β Receptor Type II in the Presence of Mutated Apc, Promoting Colorectal Cancer Proliferation.
Specimen part
View SamplesGene expression profiles of Cbfb-deficient and control Treg cells were compared.
Indispensable role of the Runx1-Cbfbeta transcription complex for in vivo-suppressive function of FoxP3+ regulatory T cells.
Sex, Age, Specimen part
View SamplesHigh levels of Hes1 expression are frequently found in BCR-ABL-positive chronic myelogenous leukemia in blast crisis (CML-BC). In mouse bone marrow transplantation (BMT) models, co-expression of BCR-ABL and Hes1 induces CML-BClike disease; however the underlying mechanism remained elusive. Here, based on gene expression analysis, we show that MMP-9 is upregulated by Hes1 in common myeloid progenitors (CMPs). Analysis of promoter activity demonstrated that Hes1 upregulated MMP-9 by activating NF-kB. Analysis of 20 samples from CML-BC patients showed that MMP-9 was highly expressed in three, with two exhibiting high levels of Hes1 expression. Interestingly, MMP-9 deficiency impaired the cobblestone area-forming ability of CMPs expressing BCR-ABL and Hes1 that were in conjunction with a stromal cell layer. In addition, these CMPs secreted MMP-9, promoting the release of soluble Kit-ligand (sKitL) from stromal cells, thereby enhancing proliferation of the leukemic cells. In accordance, mice transplanted with CMPs expressing BCR-ABL and Hes1 exhibited high levels of sKitL as well as MMP-9 in the serum. Importantly, MMP-9 deficiency impaired the development of CML-BClike disease induced by BCR-ABL and Hes1 in mouse BMT models. The present results suggest that Hes1 promotes the development of CML-BC, partly through MMP-9 upregulation in leukemic cells.
Hes1 promotes blast crisis in chronic myelogenous leukemia through MMP-9 upregulation in leukemic cells.
Specimen part
View SamplesRearrangements involving the NUP98 gene resulting in fusions to several partner genes occur in acute myeloid leukemia and myelodysplastic syndromes. This study demonstrates that the second FG repeat domain of the NUP98 moiety of the NUP98-HOXA9 fusion protein is important for its cell immortalization and leukemogenesis activities. We demonstrate that NUP98-HOXA9 interacts with MLL via this FG repeat domain and that, in the absence of MLL, NUP98-HOXA9-induced cell immortalization and leukemogenesis are severely inhibited. Molecular analyses indicate that MLL is important for the recruitment of NUP98-HOXA9 to the HOXA locus and for NUP98-HOXA9-induced HOXA gene expression. Our data indicate that MLL is crucial for NUP98-HOXA9 leukemia initiation.
MLL is essential for NUP98-HOXA9-induced leukemia.
No sample metadata fields
View Samples