Gan mice express Wnt1, Ptgs2, and Ptges, which develop inflammation-associated gastric tumors (Oshima et al, Gastroenterology 131: 1086, 2006). We examined the role of MyD88 in tumorigenesis by construction of Myd88-/- Gan mice and bone marrow transplantation into Gan mice from Myd88-/- mice. Overall design: Total RNA was prepared from wild-type normal glandular stomach (n=3: WT 1–WT 3), B6 C2mE mice (n=3: C2mE 1–C2mE 3), B6 Gan mice (n=3: Gan1–Gan3), B6 Gan MyD88-/- mice (n=3: Gan 1 (MyD88-/-)–Gan 3 (MyD88-/-)), and B6 bone marrow transplanted Gan mice from Myd88-/- mice (n=3: BMT-Gan 1 (from MyD88-/-)–BMT-Gan 3 (from MyD88-/-)). We used Illumina HiSeq 2000, and examined expression profiles.
NF-κB-induced NOX1 activation promotes gastric tumorigenesis through the expansion of SOX2-positive epithelial cells.
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View SamplesNoxo1, a component of NADPH oxidase 1 (NOX1) complex, is upregulated in gastric cancer cells in a inflammation-dependent manner, and plays an important role in tumorigenesis (Oncogene, 33: 3820, 2014). To examine the mechanism of NOX1/ROS signaling in tumorigenesis, MKN45 gastric cancer cells were treated with apocynin, an inhibitor for NOX, and their gene expression was examined by RNA sequencing. Based on expression data, Sox2 was shown to be suppressed by apocynin, suggesting a role of Sox2 in a inflammation-associated gastric tumorigenesis. Overall design: Total mRNA expression profiles of Apocynin administrated MKN45 in 2 trials.
NF-κB-induced NOX1 activation promotes gastric tumorigenesis through the expansion of SOX2-positive epithelial cells.
Specimen part, Cell line, Treatment, Subject
View SamplesApc(D716) mutant mice develop benign intestinal adenoma, while Apc(D716) and p53 R270H compound mutant mice develop invasive adenocarcinoma in the intestine. We examined expression profile of tumor-derived organoids using Apc(D716), Apc(D716) p53 Null, Apc(D716) p53 R270H mutant mice by RNA sequencing, and identified mutant p53-induced gene set. Overall design: Total RNA was extracted from Apc(D716) p53(+/+) tumor organoids, Apc(D716) p53(flox/flox) tumor organoids, and Apc(D716) p53(M/M) tumor organoids. For each genotype, two mice were used and organoids were prepared independently. p53(flox) allele is null mutation, whereas p53(M) allele carrys R270H mutation. We used Illumina HiSeq 2500, and examined expression profiles.
Intestinal cancer progression by mutant p53 through the acquisition of invasiveness associated with complex glandular formation.
Specimen part, Cell line, Subject
View SamplesTo investigate why dipeptides accumulate in immature CML cells, we examined upstream gene expression patterns. We isolated the most primitive long-term stem cells, short-term stem cells, and KLS- progenitor cells from healthy littermate control and CML-affected mice and performed gene expression profiling using next-generation RNA-sequencing. Overall design: Gene expression profiles of the most primitive long-term (LT) stem cells (CD150+CD48-CD135-KLS+ cells), short-term (ST) stem cells (CD150-CD48-CD135- KLS+ cells), and KLS- progenitor cells from healthy littermate control and CML-affected mice
Dipeptide species regulate p38MAPK-Smad3 signalling to maintain chronic myelogenous leukaemia stem cells.
No sample metadata fields
View SamplesA frequently used experimental model of chronic pancreatitis (PC) recapitulating human disease is repeated injection of cerulein to mice. We found that two common substrains of C57BL/6 , C56BL/6J (Jackson) and C57BL/6NHsd (Harlan), exhibit different degree of CP with C57BL/6J beeing more susceptible to repetitive cerulein induced CP. The goal of this study was to identify genes associated with CP and also to identify genes differentially regulated between two substrains as candidates for the CP progression.
Differences in the degree of cerulein-induced chronic pancreatitis in C57BL/6 mouse substrains lead to new insights in identification of potential risk factors in the development of chronic pancreatitis.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesGprc5b, a retinoic acid-inducible orphan G proteincoupled receptor, is a member of the group C metabotropic glutamate receptor family. Its function is unknown. However, recent evidence suggests that it binds Frizzled Wnt receptors and may activate noncanonical Wnt signaling pathways. Here we report the discovery of a brain-enriched C-terminal splice variant of Gprc5b, Gprc5b_v2, by cDNA microarray and RT-PCR analyses. The variant appeared to have been downregulated in the brains of learning/memory-deficient p97FE65 null mice. Despite the fact that the mice had been backcrossed with the C57Bl/6J strain for more than ten generations, Gprc5b and other genes surrounding the FE65 locus on mouse chromosome 7 were retained from the 129-derived ES cells used to generate the knockout line. The differential splicing is unlikely due to FE65 function, as originally suspected, as Gprc5b_v2 expression is also downregulated in the brains of 129/Sv substrains in comparison to C57Bl/6J mice. Further characterization revealed the expression of both Gprc5b_v2 and the previously described variant, Gprc5b_v1, in neurons. Interestingly, Gprc5b_v2 mRNA levels increase with neuronal maturation, paralleling the expression of synaptic proteins involved in the regulation of synaptic plasticity. Finally, we report evidence that both Gprc5b_v2 and Gprc5b_v1 regulate neurite outgrowth. These results are consistent with a putative function of Gprc5b in noncanonical Wnt signaling, which play roles in the regulation of neuronal morphology, and the formation and modulation of neuronal circuitry.
A flanking gene problem leads to the discovery of a Gprc5b splice variant predominantly expressed in C57Bl/6J mouse brain and in maturing neurons.
No sample metadata fields
View SamplesCD133 (Prominin1) is pentaspan transmembrane glycoprotein expressed in several stem cell populations and cancers. Reactivity with an antibody (AC133) to a glycoslyated form of CD133 has been widely used for the enrichment of cells with tumor initiating activity in xenograph transplantation assays. We have found by fluorescence-activated cell sorting that increased AC133 reactivity in human embryonic stem cells, colon cancer and melanoma cells is correlated with increased DNA content and reciprocally, that the least reactive cells are in the G1/G0 portion of the cell cycle. Continued cultivation of cells sorted on the basis of high and low AC133 reactivity results in a normalization of the cell reactivity profiles indicating that cells with low AC133 reactivity can generate highly reactive cells as they resume proliferation. The association of AC133 with actively cycling cells may contribute to the basis for enrichment for tumor initiating activity.
Cell cycle-dependent variation of a CD133 epitope in human embryonic stem cell, colon cancer, and melanoma cell lines.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
A gene expression signature of acquired chemoresistance to cisplatin and fluorouracil combination chemotherapy in gastric cancer patients.
No sample metadata fields
View SamplesThis study was conducted to identify transcriptional profiles predictive of a clinical response of metastatic gastric cancer patients to cisplatin and fluorouracil (CF) combination chemotherapy.
A gene expression signature of acquired chemoresistance to cisplatin and fluorouracil combination chemotherapy in gastric cancer patients.
No sample metadata fields
View SamplesThis study was conducted to identify dysregulated genes associated with acquired resistance to chemotherapy.
A gene expression signature of acquired chemoresistance to cisplatin and fluorouracil combination chemotherapy in gastric cancer patients.
No sample metadata fields
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