Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression in human endometrial cancer tissues and serous papillary endometrial cancer cell line, SPAC-1L, treated by STAT1-siRNA and/or IFN-gamma

ABSTRACT: Endometrial cancer is one of the most common gynecologic malignancies, and patients with high grade disease, especially serous papillary subtype (SPEC) are often related to the poor outcomes. Recent genome-wide analyses have revealed that SPEC exhibits gene expression profiles that are distinct from the endometrioid histologic subtype; therefore, it is important to identify the SPEC driver genes or pathways responsible for the inherently aggressive phenotypes and to develop SPEC-specific therapies to target these driver genes or pathways. Through array-based analysis and immunohistochemical staining of human endometrial cancer tissue, STAT1 is identified high expressed, and can distinguish SPEC from other subtypes of endometrial cancer. In vitro and in vivo experiments show STAT1 role as a pro-survival factor in SPEC. STAT1 was identified as a master gene modulating “transcriptional pro-survival pathways” to enhance multiple malignant characteristics These finding may suggest that targeting of STAT1, the SPEC driver gene, may provide the means to improve poor outcomes for patients with SPEC.

ORGANISM(S): Homo sapiens

PROVIDER: GSE56026 | GEO | 2014/03/20

SECONDARY ACCESSION(S): PRJNA242255

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression in human endometrial cancer tissues and serous papillary endometrial cancer cell line, SPAC-1L, treated by STAT1-siRNA and/or IFN-gamma

Project description:Endometrial cancer is one of the most common gynecologic malignancies, and patients with high grade disease, especially serous papillary subtype (SPEC) are often related to the poor outcomes. Recent genome-wide analyses have revealed that SPEC exhibits gene expression profiles that are distinct from the endometrioid histologic subtype; therefore, it is important to identify the SPEC driver genes or pathways responsible for the inherently aggressive phenotypes and to develop SPEC-specific therapies to target these driver genes or pathways. Through array-based analysis and immunohistochemical staining of human endometrial cancer tissue, STAT1 is identified high expressed, and can distinguish SPEC from other subtypes of endometrial cancer. In vitro and in vivo experiments show STAT1 role as a pro-survival factor in SPEC. STAT1 was identified as a master gene modulating “transcriptional pro-survival pathways” to enhance multiple malignant characteristics These finding may suggest that targeting of STAT1, the SPEC driver gene, may provide the means to improve poor outcomes for patients with SPEC. We used microarrays to clarify the changes of gene expression along with STAT1-siRNA treatment and to confirm whether there are any changes on genes expression related to STAT1 pathway. We also used the microarray data to clarify genes signatures which can distinguish subtype of human endometrial cancers.

2014-03-20 | E-GEOD-56026 | biostudies-arrayexpress

Transcription profiling of human xenografts produced from an endometrial cell line treated with bevacizumab (Avastin)

Project description:Microarrays were used to determine the efficacy of bevacizumab (a monoclonal antibody against the vascular endothelial growth factor and its receptors.) on endometrial cancer cells. Endometrial cancer is the most frequent gynecologic cancer in women. Long term outcomes for patients with advanced stage or recurrent disease are poor. Targeted molecular therapy against the vascular endothelial growth factor (VEGF) and its receptors constitute a new therapeutic option for these patients. The goal of our work was to assess the potential effectiveness of inhibition of VEGF/VEGFR signaling in a xenograft model of endometrial cancer using bevacizumab (Avastin, a humanized antibody against VEGFA). We also aimed to identify molecular markers of sensitivity or resistance to this agent. We show that bevacizumab retards tumor growth in athymic mice by inhibiting molecular components of signaling pathways that sustain cell survival and proliferation. We also demonstrate that resistance to bevacizumab may involve up-regulation of antiapoptotic genes and certain proto-oncogenes. Experiment Overall Design: Human xenografts produced from endometrial cell line, grown in athymic mice, were treated in vivo with bevacizumab.

2009-11-16 | E-GEOD-18195 | biostudies-arrayexpress

Changes in proteomics of endometrial tissue during secretion of polycystic ovary syndrome may affect endometrial receptivity

Project description:Polycystic ovary syndrome (PCOS) is one of the most common endocrinopathies among fertile women. PCOS patients have been confirmed to be accompanied by an increased risk of pregnancy complication, and the exact cause is still unclear. Many factors may cause this situation, and impaired endometrial receptivity could be responsible for adverse pregnancy outcomes in PCOS. Unfortunately, there were still few researches about the molecular mechanisms regarding impaired endometrial receptivity. So we designed this study to explore the secretory endometrial proteome in PCOS patients.

2022-06-09 | PXD024735 | Pride

Effects of bevacizumab (avastin) in mouse model of endometrial cancer

2009-09-22 | GSE18195 | GEO

Endometrial gene expression differences in women with coronavirus disease 2019

Project description:Objective: To study the potential effect of COVID-19 on the endometrium of affected symptomatic women. Design: Preliminary study of the endometrial transcriptomes in women with COVID-19 through RNA sequencing. Setting: Hospital and university laboratories. Subjects: Women with COVID-19 lacking SARS-CoV-2 infection in endometrial tissue. Intervention/Exposure: Endometrial biopsy collection. Main outcomes measures: Endometrial gene expression and functional analysis of patients with COVID-19 versus uninfected individuals. Results: COVID-19 systemic disease alters endometrial gene expression in 75% of women, with patients exhibiting a preponderance of 163 up-regulated (e.g., UTS2, IFI6, IFIH1, BNIP3) and 72 down-regulated genes (e.g., CPZ, CDH3, IRF4) (FDR<0.05). A total of 161 dysregulated functions (36 up-regulated and 125 down-regulated) were typically enriched in COVID-19 endometria, including upregulation in pathways involved in response to virus and cytokine inflammation, highlighting upregulation of a COVID-19 response pathway. Conclusion: COVID-19 affects endometrial gene expression despite the absence of SARS-CoV-2 particles in endometrial tissues.

2024-04-22 | GSE202553 | GEO

Transcriptomic profiling of patient-derived endometrial cancer organoids (Berg HF)

Project description:Patient-derived endometrial cancer organoids. The data was used to compare gene expression profile between organoids, and to explore whether an organoid-derived gene signature could predict disease outcomes in independent patient cohorts.

2021-07-16 | E-MTAB-10664 | biostudies-arrayexpress

Endometrial DNA methylation signatures of cattle fertility

Project description:This study was done to identify endometrial DNA methylation marks that can be associated with pregnancy outcomes in postpartum cows at the time of breeding. Results showed that postpartum cows that could become pregnant could be distinguishable based on their endometrial DNA methylation patterns at the time of breeding.

2023-12-25 | GSE248185 | GEO

Derivation of endometrial gland organoids from term placenta

Project description:A limitation of current methods for the generation of endometrial gland organoids is their reliance on decidua isolated from endometrial biopsies or elective abortion. Here we report the establishment of endometrial gland organoids from decidua isolated from term placental membranes. These organoids express typical markers of glandular epithelia such as E-cadherin, Laminin and Cytokeratin 7, and can be propagated in cell culture through multiple passages. Additionally, we identified potential survival factors for the co-culture of organoids and endometrial stromal fibroblasts. These modifications facilitate the generation of patient-specific endometrial gland organoids with known pregnancy outcomes.

2020-09-03 | GSE157380 | GEO

Amplification of 1q32.1 refines the molecular classification of endometrial carcinoma: SNP array

Project description:The experiment aimed at refining the classification of endometrial cancer by profiling somatic copy number aberrations (SCNAs). SCNAs affecting chromosome 1q32.1 significantly correlated with worse survival and functional validation of a plausible oncogene showed MDM4 as an oncogenic driver in 1q32.1 and a putative therapeutic target for NSMP ECs.

2019-07-27 | E-MTAB-5908 | biostudies-arrayexpress

LATS1/2 Loss Promote Tumor Immune Evasion in Endometrial Cancer through Downregulating MHC-I Expression

Project description:LATS1/2 is frequently mutated and down-regulated in endometrial cancer (EC), but the contribution of LATS1/2 to endometrial tumor progression remains unclear. Here, we discovered an unexpected role of LATS1/2 in regulating MHC class I expression in EC. We demonstrate that the knockout of LATS1/2 in EC cells resulted in significant down-regulation of multiple genes of MHC/HLA Class I family and leaded to insensitivity to tumor immunotherapy. Furthermore, we found that the regulation of LATS1/2 on MHC/HLA expression does not depend on the classical Hippo pathway but on their direct interaction with STAT1 to phosphorylate STAT1 to promote STAT1 accumulating and moving into the nucleus to enhance the transcriptional activation of IRF1/NLRC5 on MHC-I. The kinase-dead mutant LATS1/2 attenuates STAT1 phosphorylation at Ser727. The expressions of LATS1/2, MHC-I, CD8A and p-STAT1（S727）are positive correlation in tissues of EC confirming our findings furtherly. Furthermore, LATS1/2 expression was negatively correlated with tumor stage in EC tissues. These findings reveal novel molecular mechanisms underlying tumor immunogenicity deficiency and elucidate the potential immunotherapy biomarker targeting LATS1/2 in EC.

2024-02-28 | GSE241847 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data