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Gene expression profiles of ovarian cancer cells by inhibiting Hh signaling

ABSTRACT: Analysis of gene expression levels in response to inhibition of Hh signaling in ovarian cancer cells using a cDNA microarray technique. Results suggest that 208 genes (50.5%) were up-regulated and 204 gene (49.5%) were down-regulated after GANT61 treatment.The focal adhesion and ECM-receptor interaction cross-talk in SKOV3 cells after treatment with GANT61, and the expression change of “focal adhesion” related genes play an important role in the processes of response to GANT61-treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE53464 | GEO | 2014/01/15

SECONDARY ACCESSION(S): PRJNA232061

REPOSITORIES: GEO

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Gene expression profiles of ovarian cancer cells by inhibiting Hh signaling

Project description:Analysis of gene expression levels in response to inhibition of Hh signaling in ovarian cancer cells using a cDNA microarray technique. Results suggest that 208 genes (50.5%) were up-regulated and 204 gene (49.5%) were down-regulated after GANT61 treatment.The focal adhesion and ECM-receptor interaction cross-talk in SKOV3 cells after treatment with GANT61, and the expression change of “focal adhesion” related genes play an important role in the processes of response to GANT61-treatment. SKOV3 cells were treated with GANT61 (20 μM for 60 hr) and control vehicle DMSO, respectively.

2014-01-15 | E-GEOD-53464 | biostudies-arrayexpress

Illumina RNA-seq of Human rhabdomyosarcoma Rh36 cell mouse xenograft tumors: effect of RITA, GANT61 and RITA/GANT61 combination treatments on xenograft tumor growth

Project description:Overactivation of the Hedgehog (HH) signaling pathway is implicated in many cancers. In this study, we demonstrate that the small molecule RITA, a p53 activator, effectively downregulates HH signaling in human medulloblastoma and rhabdomyosarcoma cells irrespective of p53. This is mediated by a ROS-independent activation of the MAP kinase JNK. We also show that in vitro RITA sensitized cells to the GLI antagonist GANT61, as co-administration of the two drugs had more pronounced effects on cell proliferation and apoptosis. In vivo administration of RITA or GANT61 suppressed rhabdomyosarcoma xenograft growth in nude mice; however, co-administration did not further enhance tumor suppression, even though cell proliferation was decreased. RITA was more potent than GANT61 in downregulating HH target gene expression; surprisingly, this suppressive effect was almost completely eliminated when the two drugs were administered together. Notably, RNA-seq demonstrated a broader response of pathways involved in cancer cell growth in the combination treatment, providing a plausible interpretation for tumor reduction in the absence of HH signaling downregulation.

2020-11-12 | GSE161235 | GEO

Inhibition of Hedgehog Signaling Pathway Impairs Cancer Cell Growth via Promotion of Autophagy

Project description:Analysis of gene expression levels in response to inhibition of Hh signaling in ovarian and glioma cancer cells using a cDNA microarray technique. Microarray analyses revealed that differentially expressed genes (DEGs) in human cancer cells are enriched in the senescence and autophagy pathways in response to the inhibition of Hh signaling. Further investigations showed that inhibition of Hh signaling induced autophagy.. ES2 and H4 cells were treated with GANT61 (20 M-NM-<M for 32hr and 48hr) and control vehicle DMSO, respectively.

2014-06-15 | E-GEOD-54936 | biostudies-arrayexpress

Inhibiting Hh signaling in Gli1+ osteogenic progenitors alleviates TMJOA

Project description:Inhibiting Hh signaling in Gli1+ osteogenic progenitors alleviates TMJOA

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Identification of genetic targets of Hh signaling in Drosophila

Project description:Paracrine Hedgehog (Hh) signaling regulates growth and patterning in many Drosophila organs. We mapped chromatin binding sites for Cubitus interruptus (Ci), the transcription factor that mediates outputs of Hh signal transduction, and we analyzed transcription profiles of control and mutant embryos to identify genes that are regulated by Hh. Putative targets we identified include several Hh pathway components, most previously identified targets, and many targets that are novel. Analysis of expression patterns of pathway components and target genes gave evidence of autocrine Hh signaling in the optic primordium of the embryo. And, every Hh target we analyzed that is not a pathway component appeared to be regulated by Hh in a tissue-specific manner. We present evidence that Hh-dependent tissue specificity is dependent upon transcription factors that are Hh-independent, suggesting that “pre-patterns” of transcription factors partner with Ci to make Hh-dependent gene expression position-specific.

2010-11-03 | GSE24028 | GEO

Identification of genetic targets of Hh signaling in Drosophila

2010-11-03 | E-GEOD-24028 | biostudies-arrayexpress

GLI transcriptional repression is inert prior to HH pathway activation

Project description:Purpose: Most Hedgehog responsive gene expression is mediated through GLI de-repression. Additionally GLI -repression is proposed to play roles in limb pre-patterning before HH pathway activation. This study evaluates if GLI repression is established prior to HH pathway activation. Methods: To determine if GLI-repression is established prior to pathway activation, we used genomic approaches to study GLI-mediated repression using the mouse developing limb as a model. We identified pre-HH (E9.25, 21-23S) and post-HH (E10.5, 32-25S) GLI3 binding regions using CUT&RUN for endogenous FLAG-tagged GLI3 proteins. Using a combination of ChIP-seq, CUT&RUN, CUT&Tag, ATAC-seq and RNA-seq, we tested whether loss of Gli3 prior to HH signaling was able to de-repress genes and enhancers, as it does after HH signaling. Results: Prior to HH signaling, GLI3 binds to poised, accessible regions with histone deacetylase (HDAC) proteins, similar to post-HH signaling. Despite GLI3 binding to most regions as it does in the post-HH limb, loss of Gli3 is unable to prematurely active target genes or enhancers. Furthermore, we find that GLI3-dependent chromatin compaction does not occur until roughly 10 hours after HH signaling would have normally been induced. Collectively, these results support that GLI repressor proteins are inert prior to HH pathway activation.

2022-01-21 | GSE178838 | GEO

Sonic Hedgehog inhibitors cyclopamine and GANT61 effect on HT-29 cells

Project description:Analysis of gene expression levels in response to inhibition of Hh signaling in HT-29 cells using a cDNA microarray technique. Microarray analyses revealed that different genes after treatment with both cyclopamine (an antagonist of SMO) and GANT61 (a specific, small-molecular molecule inhibitor of Glis).

2021-06-22 | GSE116218 | GEO

Transcriptional Profiling of Hh-Treated Embryoid Bodies

Project description:This experiment was specifically designed to measure neural targets of Shh signaling, we sought to profile the genes upregulated by Hh signaling in the ventral neural tube to obtain a valid dataset. To obtain ventral-specific markers, we generated retinoic acid-treated EBs grown in the presence or absence of HH-Ag. We did not observe induction of ventral Hh markers in RA-treated constitutive Gli1FLAG EBs and used these for the control, baseline set. The presence of FoxA2, Nkx2.9 and Nkx6.1 amongst the top 10 genes based on expression levels suggests that profiling significantly enriches for Hh-dependent cell types. As expected, the benchmark standard Gli1 was not up-regulated in our array, since it is constitutively expressed in the control as well. Keywords: neural progenitors, embryoid bodies, differentiation, Hedgehog, retinoic acid

2007-04-20 | GSE4936 | GEO

Phosphoproteomics of induced and inhibited early Hh signaling in human medulloblastoma cells

Project description:Aberrant sonic hedeghog signaling is implicated in the development of various cancer entities such as medulloblastoma. The canonical signaling cascade has been studied for years. Activation of GLI transcription factors was revealed as the driving force upon pathway activation. Phosphorylation by Proteinkinase A, Casein Kinase 1 and Glycogen Synthase Kinase 3 β has been found to influence the degradation of the GLI transcription factors. However, the deeper role of phosphorylation in the signal transduction remains unclear. We, therefore, applied comprehensive HPLC-MS/MS based phosphoproteomics to reveal phosphorylation dynamics underlying the chemical activation and inhibition of sonic hedgehog signaling in human medulloblastoma cells. Human medulloblastoma cells were treated with SAG (Hh pathway induction) and Vismodegib (Hh pathway inhibition) for 5 and 15 minutes. Our phosphoproteomic profiling revealed a central role of phosphorylation in the regulation of ciliary assembly, trafficking and signal transduction after 5 minutes treatment. ERK/MAPK signaling besides protein kinase A signaling and mTOR signaling were differentially regulated. Activation of Polo-like kinase 1 and inhibtion of Caseinkinase 2A1 was characteristic for Vismodegib treatment while SAG treatment induced Aurora kinase A activity. Distinctive phosphorylation of central players of sonic Hh signaling such as Smoothened, SUFU, Gli2 and Gli3 was obtained after 15 minutes treatment.

2021-09-08 | PXD013408 | Pride

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