Role of TCF19 in endometrial cancer
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA902322 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22311785_1.fastq.gz | Fastqsanger.gz | |||
| SRR22311785_2.fastq.gz | Fastqsanger.gz | |||
| SRR22311786_1.fastq.gz | Fastqsanger.gz | |||
| SRR22311786_2.fastq.gz | Fastqsanger.gz | |||
| SRR22311787_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 16 |
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Project description:In our study, TCF19 was found to be upregulated in microsatellite instability (MSI) endometrial cancer and was associated with poor prognosis and immune exhaustion signature. Elevated TCF19 enhanced cell proliferation and migration, which promoted tumorigenicity under non-immunological background; Moreover, tumoral TCF19 expression could also promote CD8+T cell exhaustion in tumor immune microenvironment, which facilitated immune escape and tumor development. Therefore, TCF19 could be a promising biomarker and effective therapeutic target for MSI endometrial cancer.
2023-08-11 | GSE218096 | GEO
Project description:In our study, TCF19 was found to be upregulated in microsatellite instability (MSI) endometrial cancer and was associated with poor prognosis and immune exhaustion signature. Elevated TCF19 enhanced cell proliferation and migration, which promoted tumorigenicity under non-immunological background; Moreover, tumoral TCF19 expression could also promote CD8+T cell exhaustion in tumor immune microenvironment, which facilitated immune escape and tumor development. Therefore, TCF19 could be a promising biomarker and effective therapeutic target for MSI endometrial cancer.
2023-08-11 | GSE218098 | GEO
Project description:Chromatin Immunoprecipitation(ChIP)-seq of TCF19 in endometrial cancer cells
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Project description:RNA sequencing of TCF19 knockdown by siRNA in endometrial cancer cells
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Project description:Endometrial cancer is the most commonly diagnosed gynecologic malignancy in women after breast, lung and colorectal cancer. Despite numerous scientific advances, the incidence and mortality rate of endometrial cancer is on the rise. Considerable research effort has therefore been placed on understanding the pathogenesis of this disease to combat this growing issue. There is now emerging evidence to suggest a putative role for dysregulation of the renin angiotensin system (RAS) and in particular the (pro)renin receptor ((P)RR), in the ontogenesis of endometrial cancer. Support for this notion arises from previous literature implicating (P)RR in cancer pathophysiology (e.g., breast cancer and pancreatic carcinoma) by virtue of its role in proliferation, angiogenesis, fibrosis, migration and invasion. In view of these data, we aimed to investigate the functional role of (P)RR in human endometrial cancer progression and development. To this end, we employed an siRNA-mediated knock down approach to abrogate (P)RR expression in the immortalized endometrial epithelial cell lines; Ishikawa, AN3CA and HEC-1A to explore the role of (P)RR in cellular proliferation and cellular viability. To further extend these analyses we also carried out a sophisticated proteomic screen, that investigated the potential pathways via which (P)RR is acting in endometrial cancer physiology. These data confirmed that (P)RR is critical for endometrial cell cancer development, contributing to both its proliferative capacity and in the maintenance cell viability. This is likely mediated through proteins such as MGA, SLC4A7, SLC7A11 or DHRS2, which were reduced following (P)RR knockdown. These putative protein interactions/pathways, which rely on the presence of (P)RR, are likely to contribute to endometrial cancer progression and could therefore, represent several novel therapeutic targets in the treatment of this cancer. Finally we contend that (P)RR, in its soluble form (s(P)RR) in blood, may have substantial potential as a novel biomarker for cancer diagnosis and prognosis prediction going forward.
2022-04-23 | PXD023042 | Pride
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-08-11 | GSE218099 | GEO
Project description:Estrogen signaling through estrogen receptor alpha (ER) plays a major role in endometrial cancer risk and progression; however, the molecular mechanisms underlying ER’s regulatory role in endometrial cancer are poorly understood. In breast cancer cells, ER genomic binding is enabled by FOXA1 and GATA3, but the transcription factors that control ER genomic binding in endometrial cancer cells remain unknown. We previously identified ETV4 as a candidate factor controlling ER genomic binding in endometrial cancer cells and here we explore the functional importance of ETV4. Homozygous deletion of ETV4, using CRISPR/Cas9, led to greatly reduced ER binding at the majority of loci normally bound by ER. Consistent with the dramatic loss of ER binding, the gene expression response to estradiol was dampened for most genes. ETV4 contributes to estrogen signaling in two distinct ways; ETV4 loss impacts chromatin accessibility at some ER bound loci and impairs ER nuclear translocation. The diminished estrogen signaling upon ETV4 deletion led to decreased growth, particularly in 3D culture where hollow organoids were formed. Our results show that ETV4 plays a necessary role in estrogen signaling in endometrial cancer cells.
2019-04-23 | GSE129803 | GEO
Project description:Estrogen signaling through estrogen receptor alpha (ER) plays a major role in endometrial cancer risk and progression; however, the molecular mechanisms underlying ER’s regulatory role in endometrial cancer are poorly understood. In breast cancer cells, ER genomic binding is enabled by FOXA1 and GATA3, but the transcription factors that control ER genomic binding in endometrial cancer cells remain unknown. We previously identified ETV4 as a candidate factor controlling ER genomic binding in endometrial cancer cells and here we explore the functional importance of ETV4. Homozygous deletion of ETV4, using CRISPR/Cas9, led to greatly reduced ER binding at the majority of loci normally bound by ER. Consistent with the dramatic loss of ER binding, the gene expression response to estradiol was dampened for most genes. ETV4 contributes to estrogen signaling in two distinct ways; ETV4 loss impacts chromatin accessibility at some ER bound loci and impairs ER nuclear translocation. The diminished estrogen signaling upon ETV4 deletion led to decreased growth, particularly in 3D culture where hollow organoids were formed. Our results show that ETV4 plays a necessary role in estrogen signaling in endometrial cancer cells.
2019-04-23 | GSE129802 | GEO
Project description:Microbiota in endometrial pathology and cancer
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