VEPH1 expression in ovarian cancer cell lines and its relationship to TGF-B signaling
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE67765 | GEO | 2015/05/25
SECONDARY ACCESSION(S): PRJNA280862
REPOSITORIES: GEO
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Project description:The current study examines the functional role of VEPH1, a PH domain containing protein and the human ortholog of Drosophila melted, in ovarian cancer cell lines. Elevated VEPH1 is associated with FOXO and Hippo signaling and was found to suppress TGF-ß induced target genes. SKOV3 cell lines were established as either CdCl2 inducible Flag-tagged VEPH1 expression or mock-transfected. Gene expression profiles were then generated both with and without the presence of TGF-ß to induce TGF-ß signaling. 3 replicates per treatment group were used.
2015-05-25 | E-GEOD-67765 | biostudies-arrayexpress
Project description:Post-embryonic development of the nematode C. elegans is governed by nutrient availability. L1-stage larvae remain in a state of developmental arrest after hatching until they feed. This “L1 arrest” (or "L1 diapause") is associated with increased stress resistance, supporting starvation survival. Loss of the transcription factor daf-16/FOXO, an effector of insulin/IGF signaling, results in arrest-defective and starvation-sensitive phenotypes. We show that daf-16/FOXO regulates L1 arrest cell-nonautonomously, suggesting that insulin/IGF signaling regulates at least one additional signaling pathway. We used mRNA-seq to identify candidate signaling molecules affected by daf-16/FOXO during L1 arrest. daf-16/FOXO had overlapping but distinct effects on gene expression in L1 arrest compared to daf-2/InsR adults. Notably, dbl-1/TGF-β, a ligand for the Sma/Mab pathway, and daf-36, which encodes an upstream component of the daf-12/NHR steroid hormone signaling pathway, were up-regulated during L1 arrest in a daf-16/FOXO mutant. Using genetic epistasis analysis, we show that dbl-1/TGF-β and daf-12/NHR steroid hormone signaling pathways are required for the daf-16/FOXO arrest-defective phenotype, suggesting that daf-16/FOXO represses dbl-1/TGF-β and daf-36. The dbl-1/TGF-β and daf-12/NHR pathways have not previously been shown to affect L1 development, but we found that disruption of these pathways delayed L1 development in fed larvae, consistent with these pathways promoting development in starved daf-16/FOXO mutants. Though the dbl-1/TGF-β and daf-12/NHR pathways are epistatic to daf-16/FOXO for the arrest-defective phenotype, disruption of these pathways does not suppress starvation sensitivity of daf-16/FOXO mutants. This observation uncouples starvation survival from developmental arrest, indicating that DAF-16/FOXO targets distinct effectors for each phenotype, and revealing that inappropriate development during starvation does not cause the early demise of daf-16/FOXO mutants. Overall, this study shows that daf-16/FOXO promotes developmental arrest cell-nonautonomously by repressing pathways that promote larval development.
2016-05-27 | GSE69329 | GEO
Project description:Very little is known about how intervertebral disc (IVD) is formed or maintained. Members of the TGF-ß superfamily are secreted signaling proteins that regulate many aspects of development including cellular differentiation. We recently showed that deletion of Tgfbr2 in Col2a expressing tissue results in alterations in development of IVD annulus fibrosus. The results suggested TGF-ß has an important role in regulating development of the axial skeleton, however, the mechanistic basis of TGF-ß action in these specialized joints is not known. To understand the mechanism of TGF-ß action in IVD development, we undertook a global analysis of gene expression comparing gene expression profiles in sclerotome cultures treated with TGF-ß or BMP4. As expected, treatment with BMP4 resulted in up-regulation of cartilage marker genes including Acan, Sox 5, Sox6, and Sox9. In contrast, treatment with TGF-ß1 did not regulate expression of cartilage markers but instead resulted in up-regulation of many IVD markers including Fmod and Adamtsl2. We propose TGF-ß has two functions in IVD development: 1) to prevent chondrocyte differentiation in the presumptive IVD and 2) to promote differentiation of annulus fibrosus from sclerotome. We have identified genes that are enriched in the IVD and regulated by TGF-ß that warrant further investigation as regulators of IVD development.
2010-04-09 | GSE18648 | GEO
Project description:To analyse whether the activation of TGF-ß signalling (recombinant hTGF-ß, 5 ng/mL; PeproTech) is able to invoke a full phenotype- switch, we performed RNA sequencing of melanoma cultures from two independent melanoma cell lines at two different time point after TGF-β1 (5 ng/ml, preprotech).
2020-04-17 | GSE148767 | GEO
Project description:In this study, we identified a number of genes whose expression are regulated by the Hippo tumor suppressor pathway. To disrupt Hippo signaling in the mouse heart, we inactivated the single mammalian Salv ortholog using a Salv conditional null allele and the Nkx2.5 cre allele that directs cardiac cre activity. Total RNA from embryonic hearts were used for expression profiling of 17,455 unique genes. Genes transcriptionally regulated by the Hippo pathway during cardiogenesis were identifed through expression profiling of 17,455 unique genes in Salvador mutant (Salv CKO) embryonic hearts. Total RNA from E9.5-stage hearts were pooled into biological replicate samples (2 control and 2 Salv CKO) and were used to generate expression profiles.
2011-02-12 | E-GEOD-27259 | biostudies-arrayexpress
Project description:In this study, we identified a number of genes whose expression are regulated by the Hippo tumor suppressor pathway. To disrupt Hippo signaling in the mouse heart, we inactivated the single mammalian Salv ortholog using a Salv conditional null allele and the Nkx2.5 cre allele that directs cardiac cre activity. Total RNA from P8-stage hearts were used for expression profiling. Genes transcriptionally regulated by the Hippo pathway during cardiogenesis were identifed through expression profiling in Salvador mutant (Salv CKO) neontate hearts. Total RNA from postnatal day 8 (P8)-stage hearts was purified to generate biological replicate samples (2 control and 2 Salv CKO) and generate expression profiles. 3 technical replicates were used for each sample.
2015-05-12 | E-GEOD-44103 | biostudies-arrayexpress
Project description:By performing oligonucleotide microarray analysis the role of Smad4 in response to TGF-ß was evaluated in established MDA-MB-468 Smad4 negative and positive clones that were treated with TGF-ß for different time points. Keywords: time-course
2006-04-25 | GSE2567 | GEO
Project description:Background: Penicillins inhibit cell wall synthesis; therefore, H. pylori must be dividing for these antibiotics to be effective. Identifying growth responses to varying medium pH may allow design of more effective treatment regimens. Aim: To determine the effect of acidity on bacterial growth and the bactericidal efficacy of ampicillin. Methods: H. pylori were incubated in dialysis chambers suspended in 1.5L of media at various pHs with 5mM urea, with or without ampicillin, for 4, 8 or 16 hours, thus mimicking unbuffered gastric juice. Changes in gene expression, viability and survival were determined. The bacterial load of H. pylori infected gerbils was determined with and without profound acid inhibition. Results: At pH 3.0, but not at pH 4.5 or 7.4, there was decreased expression of ~400 genes, including many cell envelope biosynthesis, cell division genes and penicillin-binding proteins. In the presence of ampicillin, viability and survival declined at pH 4.5 and 7.4 but not at pH 3.0. Profound acid inhibition of H. pylori infected gerbils increased the antral bacterial load >3 fold, showing that elevation of intragastric pH stimulated growth. Conclusions: Ampicillin is bactericidal at pH 4.5 and 7.4, but not at pH 3.0, due to decreased expression of cell envelope and division genes at pH 3.0. Therefore, at pH 3.0, the pH at the gastric surface, the bacteria are non-dividing and persist with ampicillin treatment. A more effective inhibitor of acid secretion that maintains gastric pH near neutrality for 24 hours/day should enhance the efficacy of triple therapy and of amoxicillin, even allowing dual therapy for H. pylori eradication.
2012-09-30 | GSE39512 | GEO
Project description:In this study, we identified a number of genes whose expression are regulated by the Hippo tumor suppressor pathway. To disrupt Hippo signaling in the mouse heart, we inactivated the single mammalian Salv ortholog using a Salv conditional null allele and the Nkx2.5 cre allele that directs cardiac cre activity. Total RNA from P8-stage hearts were used for expression profiling.
2015-05-12 | GSE44103 | GEO
Project description:In this study, we identified chromatin regions bound by YAP, a major effector of the Hippo tumor suppressor pathway. To disrupt Hippo signaling in the mouse heart, we inactivated the single mammalian Salv ortholog using a Salv conditional null allele and and tamoxifen inducible Myh6-cre/Esr1 allele, Cre activity was induced with 4 consecutive intraperitoneal (i.p.) or subcutaneous injections of tamoxifen from P7-P10.
2019-09-25 | GSE46529 | GEO