MRNA expression files of spermatogonial stem cells in response to Bisphnel A
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE89551 | GEO | 2018/11/04
REPOSITORIES: GEO
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Project description:Purpose:The study aimed to recognize potential molecular targets and signal pathways whereby phenolic environmental estrogen promotes the proliferation of uterine leiomyoma cells Methods:Primary cultured cell lines were treated with 0.1% DMSO, 10.0 μmol/L BPA, and 32.0 μmol/L NP for 48 h before RNA-seq was performed. Differentially expressed genes affected by BPA and NP were selected. Then, Gene Ontology (GO) enrichment, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, and Protein-protein Interaction (PPI) analysis were performed. Quantitative real-time polymerase chain reaction (q-PCR) was used to verify the differentially expressed genes Results:In comparison with the control group, 739 differentially expressed mRNAs were identified in the BPA intervention group and the NP intervention group. GO enrichment analysis results show that the most enriched GO terms were connective tissue development and G1/S transition of mitotic cell cycle, and extracellular matrix. The results of KEGG enrichment analysis showed that differentially expressed mRNA was enriched mainly in three primary pathways, including environmental information processing, human diseases, and cellular processes. The cell cycle, PI3K-Akt signaling pathway, pathways in cancer, and TGF-beta signaling pathway are significantly enriched. Conclusions:Phenolic environmental estrogens may promote the proliferation and cell cycle progression of uterine leiomyoma cells through rapid non-genomic ER signaling, which leads to disordered cell cycle regulation and accelerates the transition of the cell cycle from G0/G1 phase to S phase. In addition, as an external harmful stimulant, phenolic estrogen promotes the upregulation of inflammatory factors in uterine leiomyomas.
2021-04-27 | GSE173334 | GEO
Project description:Purpose: finding differential transcripts usage in environmentally harzardous chemical, bisphenol A (BPA) in human retinal cells Methods: transcriptome analysis by the RNA-seq via mRNA pull-down Results: We found that BPA increases cellular toxicity by the increasing of early apoptotic pathway in Y79 cells. Also, over thounds of retained intron events were detected from the RNA-seq analysis. Conclusions: Bisphenol A (BPA) increases early cytotoxic effects in Y79 cells through the early apoptotic pathway and changes the context of trascript through the splicing regulation mechanisms.
2021-02-16 | GSE146255 | GEO
Project description:To further explore the mechanism involved in sACE mediated SSCs proliferation. We established microarray gene expression profiles with or without captopril treatment in cultured SSCs and identified 651 differentially expressed genes (Fold Change>2, P<0.05). Among them, 297 genes were remarkably upregulated and 354 genes were downregulated in three comparison groups after captopril treatment.Then bioinformatical analysis including GO analysis and KEGG pathway analysis were performed and both of them indicated these differentially expressed genes might be involved in regulation of tyrosine phosphorylation of STAT protein, ERK1 and ERK2 cascade, MAPK signaling, Jak-STAT signaling and et al. Four MAPK signaling related genes (Pla2g12b, Cacna2d1, Dusp2, Fgf3) from this signature was quantified by real-time PCR.
2019-01-01 | GSE101752 | GEO
Project description:RNA sequence analysis identified a total of 8473 differentially expressed genes (DEGs) (3580 up-regulated, 4893 down-regulated), and GO annotation and KEGG enrichment of differential genes found that DEGS were mostly related to spermatogenesis and apoptosis. Among them, Spermatogonia stem cell (SSCs) marker genes (ITGA5, Gfra1, CD9, SOHLH1, SALL4, ID4 and FOXO1) were significantly up-regulated, differentiation spermatogenic cell marker genes (KIT, UCHL1, Ccna1, TNP1 and TXNDC2) were significantly down-regulated, and genes involved in apoptosis (Fas, CTSK, CTSB, CTSC, CTSO, caspase 3, caspase6, and caspase) were significantly up-regulated. Furthermore, the AS events in cattle-yak are significantly lower than in yak, we speculate that lack of mRNA and protein subtypes may lead to spermatogenic arrest in yak testicle.
2022-07-23 | GSE208693 | GEO
Project description:Rituximab, a monoclonal antibody against CD20, has achieved great success in the treatment of B cell lymphoma, but many patients have shown resistance to it and led to disease progression eventually. At present, the mechanism of resistance is still not clear, but we consider that it may involve the multiple genes and multiple signaling pathways. Therefore, our study aimed at searching differentially expressed genes of rituximab resistant cell lines (RRCL) by cDNA microarray, and exploring the resistant mechanism of RRCL by using the subsequent bioinformatics methods. In this study, we successfully identified seventy up-regulated genes and forty-two down-regulated genes in both two RRCL. We also isolated the MAPK signaling pathway, which was the significantly enriched pathway in resistant mechanism, through KEGG pathway analysis. Moreover, we discovered the biological behaviors of RRCL that mainly inhibit apoptosis, promote cellular proliferation, transcription and angiogenesis through Gene Ontology (GO) terms analysis. In conclusion, our results suggested that the most closely related pathway to rituximab resistance was MAPK signaling pathway, which may partly be related to its inhibiting the apoptosis of cells and promoting the proliferation of cells and vascular development. We utilized human mantle cell lymphoma cell line Jeko-1 and human Burkitt lymphoma cell line Raji to establish rituximab resistant Jeko-1/R and Raji/R cell lines. And then, in order to explore rituximab resistant mechanism, we looked for the different gene expression profile of rituximab resistant cell lines compared with the parental cell lines by cDNA microarray and carried out subsequent KEGG pathway and GO terms analysis.
2014-08-13 | E-GEOD-60327 | biostudies-arrayexpress
Project description:Sarcomas and leukemias that are characterized by FET (FUS, EWSR1, TAF15) fusion oncogenes consist of more than 20 entities. Myxoid liposarcoma, one of the most common FET sarcoma types, is defined by the FUS-DDIT3 or the less common EWSR1-DDIT3 fusion oncogene. Previously, JAK-STAT signaling have been connected to cancer stem cell properties and chemotherapy resistance in myxoid liposarcoma, but the role of FUS-DDIT3 is not known. Therefore, we treated HT1080 fibrosarcoma cells expression FUS-DDIT3 with JAK1/2 inhibitor ruxolitinib and performed RNA sequencing of treated and control cells. Additionally, we analyzed native HT1080 cells to be able to compare the induced gene expression changes due to FUS-DDIT3 expression with those induced by JAK-STAT pathway inhibition.
2022-01-14 | GSE149650 | GEO
Project description:Xenoestrogens are part of a group of agents termed endocrine disruptors because of their capacity to perturb normal hormonal actions. It has been suggested that xenoestrogens may contribute to the development of hormone-dependent cancers, such as breast and endometrial cancers. Bisphenol A (BPA) is polymerized to manufacture polycarbonate plastic and epoxy resins. Human exposure occurs when BPA leaches from plastic-lined food and beverage cans. In the present work we are aiming to determine if BPA has carcinogenic properties by using an in vitro system. For this purpose the human breast epithelial cells MCF-10F were treated with 10-3M to 10-9M BPA continuously for two weeks. The MCF-10F cells treated with 10-3M and 10-4M BPA died, indicating that these concentrations were toxic for the human breast epithelial cells. The cells treated with 10-5M to 10-9M BPA were evaluated for formation of solid masses in collagen and invasion capacity, both phenotypes that are indicators of cell transformation. MCF-10F treated with 10-5M, 10-6M, 10-7M, 10-8M and 10-9M BPA formed a high percentage of solid masses (34.6%, 20%, 42.4%, 31.8% and 32.2%, respectively). Ten passages after BPA treatments, the invasive capacities of the cells were evaluated using Boyden chambers. The invasion capacity was lower in the cells treated at high concentrations of BPA (10-5M and 10-6M), and there was an increased invasion for the cells treated at low BPA concentration (10-9M) although, in all the cases the differences were not significant to the controls. Expression and DNA methylation analyses were performed with the cells treated with 10-5M and 10-6M BPA. We found that these cells showed an increased expression of BRCA1, BARD1, CtIP, RAD51 and BRCC3, all genes involved in DNA repair, and downregulation of PDCD5 and BCL2L11 (also known as BIM), both involved in apoptosis. The upregulation of CtIP was related to hypomethylation of the promoter/exon1 of this gene. Furthermore, BPA induced silencing of BCL2L11 by hypermethylation. This is the first demonstration that BPA induces neoplastic transformation of breast epithelial cells and that aberrant DNA methylation of genes involved in DNA repair and apoptosis could be involved in the initiation of the neoplastic process.
2011-09-16 | GSE32158 | GEO
Project description:Xenoestrogens are part of a group of agents termed endocrine disruptors because of their capacity to perturb normal hormonal actions. It has been suggested that xenoestrogens may contribute to the development of hormone-dependent cancers, such as breast and endometrial cancers. Bisphenol A (BPA) is polymerized to manufacture polycarbonate plastic and epoxy resins. Human exposure occurs when BPA leaches from plastic-lined food and beverage cans. In the present work we are aiming to determine if BPA has carcinogenic properties by using an in vitro system. For this purpose the human breast epithelial cells MCF-10F were treated with 10-3M to 10-9M BPA continuously for two weeks. The MCF-10F cells treated with 10-3M and 10-4M BPA died, indicating that these concentrations were toxic for the human breast epithelial cells. The cells treated with 10-5M to 10-9M BPA were evaluated for formation of solid masses in collagen and invasion capacity, both phenotypes that are indicators of cell transformation. MCF-10F treated with 10-5M, 10-6M, 10-7M, 10-8M and 10-9M BPA formed a high percentage of solid masses (34.6%, 20%, 42.4%, 31.8% and 32.2%, respectively). Ten passages after BPA treatments, the invasive capacities of the cells were evaluated using Boyden chambers. The invasion capacity was lower in the cells treated at high concentrations of BPA (10-5M and 10-6M), and there was an increased invasion for the cells treated at low BPA concentration (10-9M) although, in all the cases the differences were not significant to the controls. Expression and DNA methylation analyses were performed with the cells treated with 10-5M and 10-6M BPA. We found that these cells showed an increased expression of BRCA1, BARD1, CtIP, RAD51 and BRCC3, all genes involved in DNA repair, and downregulation of PDCD5 and BCL2L11 (also known as BIM), both involved in apoptosis. The upregulation of CtIP was related to hypomethylation of the promoter/exon1 of this gene. Furthermore, BPA induced silencing of BCL2L11 by hypermethylation. This is the first demonstration that BPA induces neoplastic transformation of breast epithelial cells and that aberrant DNA methylation of genes involved in DNA repair and apoptosis could be involved in the initiation of the neoplastic process.
2011-03-10 | GSE27865 | GEO
Project description:Xenoestrogens are part of a group of agents termed endocrine disruptors because of their capacity to perturb normal hormonal actions. It has been suggested that xenoestrogens may contribute to the development of hormone-dependent cancers, such as breast and endometrial cancers. Bisphenol A (BPA) is polymerized to manufacture polycarbonate plastic and epoxy resins. Human exposure occurs when BPA leaches from plastic-lined food and beverage cans. In the present work we are aiming to determine if BPA has carcinogenic properties by using an in vitro system. For this purpose, the human breast epithelial cells MCF-10F were treated with 10-3M to 10-9M BPA continuously for two weeks. The MCF-10F cells treated with 10-3M and 10-4M BPA died, indicating that these concentrations were toxic for the human breast epithelial cells. The cells treated with 10-5M to 10-9M BPA were evaluated for formation of solid masses in collagen and invasion capacity, both phenotypes that are indicators of cell transformation. MCF-10F treated with 10-5M, 10-6M, 10-7M, 10-8M and 10-9M BPA formed a high percentage of solid masses (34.6%, 20%, 42.4%, 31.8% and 32.2%, respectively). Ten passages after BPA treatments, the invasive capacities of the cells were evaluated using Boyden chambers. The invasion capacity was lower in the cells treated at high concentrations of BPA (10-5M and 10-6M), and there was an increased invasion for the cells treated at low BPA concentration (10-9M), although in all the cases the differences were not significant to the controls. Expression and DNA methylation analysis were performed with the cells treated with 10-5M and 10-6M BPA. We found that these cells showed an increased expression of BRCA1, BARD1, CtIP, RAD51 and BRCC3, all genes involved in DNA repair, and downregulation of PDCD5 and BCL2L11 (also known as BIM), both involved in apoptosis. The upregulation of CtIP was related to hypomethylation of the promoter/exon1 of this gene. Furthermore, BPA induced silencing of BCL2L11 by hypermethylation. This is the first demonstration that BPA induces neoplastic transformation of breast epithelial cells and that aberrant DNA methylation of genes involved in DNA repair and apoptosis could be involved in the initiation of the neoplastic process.
2011-02-28 | GSE26884 | GEO
Project description:Most significantly affected GOs by TST stress include Cellular localization, transport and migration such as Cellular macromolecule localization (GO:0070727), Intracellular transport (GO:0046907) and Intracellular protein transport (GO:0006886), metabolic processes such as Small molecule metabolic process (GO:0044281), Cellular amide metabolic process (GO:0043603) and Lipid metabolic process (GO:0006629), neuronal cell population differentiation and proliferation such as Neurogenesis (GO:0022008), Neuron differentiation (GO:0030182), Glial cell differentiation (GO:0010001), Central nervous system development (GO:0007417), Astrocyte differentiation (GO:0048708) and Gliogenesis (GO:0042063), and cell signaling such as G-protein-coupled receptor signaling pathway (GO:0007186), Negative regulation of signaling (GO:0023057), Positive regulation of signaling (GO:0023056), Response to endogenous stimulus (GO:0009719) and Regulation of intracellular signal transduction (GO:1902531). Peptide metabolic process (GO:0006518), Peptidyl amino acid modification (GO:0018193), Regulation of steroid biosynthetic process (GO:0050810) were also significantly enriched in the TST stress-induced mice brain. Top significantly enriched Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathways by the stress response related DEGs between high-dose RE vs TST include mitogen-activated protein kinase (MAPK) signaling pathway, Chemokine signaling pathway, Neurotrophin signaling pathway, Cytokine-cytokine receptor interaction, GnRH signaling pathway, ErbB signaling pathway, Toll-like receptor signaling pathway, T cell receptor signaling pathway, B cell receptor signaling pathway, vascular endothelial growth factor (VEGF) signaling pathway, Long-term depression, NOD-like receptor signaling pathway, Insulin signaling pathway, Jak-STAT signaling pathway, Apoptosis, and mTOR signaling pathway.
2021-07-29 | GSE180884 | GEO