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GSE23748
Rattus norvegicus
30 Downloadable Samples
Affymetrix Rat Genome 230 2.0 Array (rat2302)
Description
The effects of freeze-dried tofu, a traditional Japanese soy food, were compared with those of major active soy components, protein and isoflavone, by observing physiological differences and global transcriptomes in the liver of male rats.
Publication Title
Tofu (soybean curd) lowers serum lipid levels and modulates hepatic gene expression involved in lipogenesis primarily through its protein, not isoflavone, component in rats.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Dorsomorphin is a small molecule inhibitor of type I bone morphogenic protein receptors (BMPRs). We have found that dorsomorphin affects a wide range of T cell function. In order to obtain the bigger picture of the effects of DM in T cell activation. transcriptomic analysis was performed using mouse primary CD25-CD4+ T cells with either DM (4 M) or vehicle in the presence or absence of stimulation by anti-CD3 and -CD28 antibodies.
Publication Title
Differential effects of inhibition of bone morphogenic protein (BMP) signalling on T-cell activation and differentiation.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Ascorbic acid (AA) is a powerful antioxidant and play as a cofactor for various enzymes in vivo. In this study, we investigated the effect of AA depletion on gene expression in the liver and lipid metabolism by using SMP30/GNL knockout (KO) mice which are unable to biosynthesis AA. First, we performed microarray analysis. Briefly, SMP30/GNL KO mice were weaned and divided into two groups; AA-depleted and supplemented groups, which mice were free access to water containing 1.5 g/L AA. After 4 weeks, mRNA was isolated and purified from the liver. In this study, Affymetrix GeneChip was used for microarray analysis. Actually, AA-depletion altered many gene expressions related to lipid metabolism. Especially, Cytochrome P450 7a1 (Cyp7a1), a late-limiting enzyme of bile acid biosynthesis, gene expression was significantly up-regulated. We also confirmed Cyp7a1 protein levels by Western blotting. Next, we investigated the influence of AA depletion on lipid metabolism. We examined the lipid and bile acid levels in the liver, plasma, and gallbladder from SMP30/GNL KO mice. Amount of total bile acid (TBA), free fatty acid (FA), total cholesterol (TC), triglyceride (TG), and phospholipids (PL) were measured by colorimetric method. AA depletion reduced TBA levels in the liver and gallbladder. However, FA, TC, TG, and PL in the plasma and liver were not changed by AA depletion. Although Cyp7a1 gene expression and protein levels were increased by AA depletion, amount of bile acid were reduced. Conclusively, we have shown that AA depletion reduced bile acid biosynthesis and elevated Cyp7a1 gene expression and protein levels. Thus, AA is an essential for bile acid biosynthesis pathway.
Publication Title
Ascorbic acid deficiency affects genes for oxidation-reduction and lipid metabolism in livers from SMP30/GNL knockout mice.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 11 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Invasion into deep myometrium and/or lymphovascular space is a well-known risk factor for endometrial cancer metastasis, resulting in poor prognosis. It is therefore clinically important to identify novel molecules that suppress tumor invasion. Reduced expression of the metastasis suppressor, KISS1 (kisspeptin), and its endogenous receptor, GPR54, has been reported in several cancers, but the significance of the KISS1/GPR54 axis in endometrial cancer metastasis has not been clarified. Metastin-10 is the minimal bioactive sequence of genetic products of KISS1. Clinicopathological analysis of 92 endometrial cancers revealed overall survival is improved in cancers with high expression of GPR54. Through RNAi and mousemodel analyses, metastin-10 was predicted to suppress invasion and metastasis of GPR54-expressing endometrial cancers. These data suggest that metastin-10 may induce genetic changes in the metastatic character of endometrial cancers.
Publication Title
GPR54 is a target for suppression of metastasis in endometrial cancer.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 129 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Epigenetic suppression of the TGF-beta pathway revealed by transcriptome profiling in ovarian cancer.
Sample Metadata Fields
Sex, Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 95 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Epithelial ovarian cancer is the leading cause of death among gynecologic malignancies. Diagnosis usually occurs after metastatic spread, largely reflecting vague symptoms of early disease combined with lack of an effective screening strategy. Epigenetic mechanisms of gene regulation, including DNA methylation, are fundamental to normal cellular function and also play a major role in carcinogenesis. To elucidate the biological and clinical relevance of DNA methylation in ovarian cancer, we conducted expression microarray analysis of 39 cell lines and 17 primary culture specimens grown in the presence or absence of DNA methyltransferase (DNMT) inhibitors. Two parameters, induction of expression and standard deviation among untreated samples, identified 378 candidate methylated genes, many relevant to TGF-beta signaling. We analyzed 43 of these genes and they all exhibited methylation. Treatment with DNMT inhibitors increased TGF-beta pathway activity. Hierarchical clustering of ovarian cancers using the 378 genes reproducibly generated a distinct gene cluster strongly correlated with TGF-beta pathway activity that discriminates patients based on age. These data suggest that accumulation of age-related epigenetic modifications leads to suppression of TGF-beta signaling and contributes to ovarian carcinogenesis.
Publication Title
Epigenetic suppression of the TGF-beta pathway revealed by transcriptome profiling in ovarian cancer.
Sample Metadata Fields
Sex, Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 55 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Ovarian cancer is characterized by multiple structural aberrations; most are passenger alterations which do not confer tumor growth. Like many cancers, it is a heterogeneous disease and till date, the histotype-specific copy number landscape has been difficult to elucidate. To dissect the heterogeneity of ovarian cancer and understand the pathogenesis of its various histotypes, we developed an in silico hypothesis-driven workflow to identify histotype-specific copy number aberrations across multiple datasets of epithelial ovarian cancer. In concordance with previous studies on global copy number changes, our study showed similar alterations. However, when the landscape was de-convoluted into histotypes, distinct alterations were observed. We report here a comprehensive histotype-specific copy number landscape of ovarian cancer and showed that there is genomic diversity between the histotypes; some involving well known cancer genes and some novel potential driver genes. Besides preferential occurrence of alterations in some histotypes, opposite trends of alteration were observed; such as ERBB2 amplification in mucinous but deletion in serous tumors. The landscape highlights the need for identifying histotype-specific aberrations in ovarian cancer and present potential to tailor management of ovarian cancer based on molecular signature of histotypes.
Publication Title
Histotype-specific copy-number alterations in ovarian cancer.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 42 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
Ovarian cancer is characterized by multiple structural aberrations; most are passenger alterations which do not confer tumor growth. Like many cancers, it is a heterogeneous disease and till date, the histotype-specific copy number landscape has been difficult to elucidate. To dissect the heterogeneity of ovarian cancer and understand the pathogenesis of its various histotypes, we developed an in silico hypothesis-driven workflow to identify histotype-specific copy number aberrations across multiple datasets of epithelial ovarian cancer. In concordance with previous studies on global copy number changes, our study showed similar alterations. However, when the landscape was de-convoluted into histotypes, distinct alterations were observed. We report here a comprehensive histotype-specific copy number landscape of ovarian cancer and showed that there is genomic diversity between the histotypes; some involving well known cancer genes and some novel potential driver genes. Besides preferential occurrence of alterations in some histotypes, opposite trends of alteration were observed; such as ERBB2 amplification in mucinous but deletion in serous tumors. The landscape highlights the need for identifying histotype-specific aberrations in ovarian cancer and present potential to tailor management of ovarian cancer based on molecular signature of histotypes.
Publication Title
Histotype-specific copy-number alterations in ovarian cancer.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 36 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
Ovarian clear cell carcinoma (OCCC) shows unique clinical features including an association with endometriosis and poor prognosis. We previously reported that the contents of endometriotic cysts, especially high concentrations of free iron, are a possible cause of OCCC carcinogenesis through iron-induced persistent oxidative stress. In this study, we conducted gene expression microarray analysis using 38 ovarian cancer cell lines and identified genes commonly expressed in both OCCC cell lines and clinical samples, which comprise an OCCC gene signature. The OCCC signature reproducibly predicts OCCC specimens in other microarray data sets, suggesting that this gene profile reflects the inherent biological characteristics of OCCC. The OCCC signature contains known markers of OCCC, such as hepatocyte nuclear factor-1b (HNF-1b) and versican (VCAN), and other genes that reflect oxidative stress. Expression of OCCC signature genes was induced by treatment of immortalized ovarian surface epithelial cells with the contents of endometriotic cysts, indicating that the OCCC signature is largely dependent on the tumor microenvironment. Induction of OCCC signature genes is at least in part epigenetically regulated, as we found hypomethylation of HNF-1b and VCAN in OCCC cell lines. This genomewide study indicates that the tumor microenvironment induces specific gene expression profiles that contribute to the development of distinct cancer subtypes.
Publication Title
Identification of an ovarian clear cell carcinoma gene signature that reflects inherent disease biology and the carcinogenic processes.
Sample Metadata Fields
Sex, Specimen part, Cell line, Treatment
View Samples- Homo sapiens
- 34 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Epithelial ovarian cancer is the leading cause of death among gynecologic malignancies. Diagnosis usually occurs after metastatic spread, largely reflecting vague symptoms of early disease combined with lack of an effective screening strategy. Epigenetic mechanisms of gene regulation, including DNA methylation, are fundamental to normal cellular function and also play a major role in carcinogenesis. To elucidate the biological and clinical relevance of DNA methylation in ovarian cancer, we conducted expression microarray analysis of 39 cell lines and 17 primary culture specimens grown in the presence or absence of DNA methyltransferase (DNMT) inhibitors. Two parameters, induction of expression and standard deviation among untreated samples, identified 378 candidate methylated genes, many relevant to TGF-beta signaling. We analyzed 43 of these genes and they all exhibited methylation. Treatment with DNMT inhibitors increased TGF-beta pathway activity. Hierarchical clustering of ovarian cancers using the 378 genes reproducibly generated a distinct gene cluster strongly correlated with TGF-beta pathway activity that discriminates patients based on age. These data suggest that accumulation of age-related epigenetic modifications leads to suppression of TGF-beta signaling and contributes to ovarian carcinogenesis.
Publication Title
Epigenetic suppression of the TGF-beta pathway revealed by transcriptome profiling in ovarian cancer.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples