Gene expression data from endometrial cancer patient-derived cells (PDCs) treated with estrogen/progesterone
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE127238 | GEO | 2022/02/22
REPOSITORIES: GEO
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Project description:Immune-related genes were upregulated in the metastatic PDC line (EnC-C) established from endometrial cancer specimen.
2022-02-22 | GSE127237 | GEO
Project description:Gene expression data from endometrial cancer patient-derived cells (PDCs) treated with estrogen/progesterone
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Project description:Every year more than 42,000 women die of endometrial cancer, mainly due to recurrent or metastatic disease. The presence of tumor infiltrating lymphocytes (TILs) as well as progesterone receptor (PR) positivity has been correlated with improved prognosis. This study describes two mechanisms by which progesterone inhibits metastatic spread of endometrial cancer: by stimulating T-cell infiltration and by inhibiting epithelial-to-mesenchymal cell transition (EMT). Paraffin sections from patients with (n=9) or without (n=10) progressive endometrial cancer (recurrent or metastatic disease) were assessed for the presence of CD4+ (helper), CD8+ (cytotoxic) and Foxp3+ (regulatory) T-lymphocytes and PR expression. Progressive disease was observed to be associated with significant loss of TILs and loss of PR expression. Frozen tumor samples, used for genome-wide expression analysis, showed significant regulation of pathways involved in immunosurveillance, EMT and metastasis. For a number of genes, such as CXCL14, DKK1, DKK4 and WIF1, quantitive RT-PCR was performed to verify down regulation in progressive disease. To corroborate the role of progesterone in regulating invasion, Ishikawa (IK) endometrial cancer cell lines stably transfected with PRA (IKPRA), PRB (IKPRB) and PRA+PRB (IKPRAB) were cultured in the presence/absence of progesterone (MPA) and used for genome-wide expression analysis, Boyden- and wound healing migration assays, and IHC for known EMT makers. IKPRB and IKPRAB cell lines showed MPA induced inhibition of migration and loss of the mesenchymal marker vimentin at the invasive front of the wound healing assay. Furthermore, pathway analysis of significantly MPA-regulated genes showed significant down regulation of important pathways involved in EMT, immunesuppression and metastasis: such as IL6-, TGF-β and Wnt/β-catenin signalling. Intact progesterone signaling in non-progressive endometrial cancer seems to be an important factor stimulating immunosurveillance and inhibiting transition from an epithelial to a more mesenchymal, more invasive phenotype. From 4 non-progressive and 4 progressive patients, snap-frozen endometrial cancer tumor specimens were used for microarray analysis. Gene expression data of progressive disease was compared with non-progressive disease.
2012-01-26 | E-GEOD-29436 | biostudies-arrayexpress
Project description:Every year more than 42,000 women die of endometrial cancer, mainly due to recurrent or metastatic disease. The presence of tumor infiltrating lymphocytes (TILs) as well as progesterone receptor (PR) positivity has been correlated with improved prognosis. This study describes two mechanisms by which progesterone inhibits metastatic spread of endometrial cancer: by stimulating T-cell infiltration and by inhibiting epithelial-to-mesenchymal cell transition (EMT). Paraffin sections from patients with (n=9) or without (n=10) progressive endometrial cancer (recurrent or metastatic disease) were assessed for the presence of CD4+ (helper), CD8+ (cytotoxic) and Foxp3+ (regulatory) T-lymphocytes and PR expression. Progressive disease was observed to be associated with significant loss of TILs and loss of PR expression. Frozen tumor samples, used for genome-wide expression analysis, showed significant regulation of pathways involved in immunosurveillance, EMT and metastasis. For a number of genes, such as CXCL14, DKK1, DKK4 and WIF1, quantitive RT-PCR was performed to verify down regulation in progressive disease. To corroborate the role of progesterone in regulating invasion, Ishikawa (IK) endometrial cancer cell lines stably transfected with PRA (IKPRA), PRB (IKPRB) and PRA+PRB (IKPRAB) were cultured in the presence/absence of progesterone (MPA) and used for genome-wide expression analysis, Boyden- and wound healing migration assays, and IHC for known EMT makers. IKPRB and IKPRAB cell lines showed MPA induced inhibition of migration and loss of the mesenchymal marker vimentin at the invasive front of the wound healing assay. Furthermore, pathway analysis of significantly MPA-regulated genes showed significant down regulation of important pathways involved in EMT, immunesuppression and metastasis: such as IL6-, TGF-β and Wnt/β-catenin signalling. Intact progesterone signaling in non-progressive endometrial cancer seems to be an important factor stimulating immunosurveillance and inhibiting transition from an epithelial to a more mesenchymal, more invasive phenotype.
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Project description:Different progesterone levels and timing of exposure results in different endometrial gene expression and implantation potential. Sufficient progesterone level is important to induce endometrial receptivity and endometrial expressed the most receptive stage after exposure to progesterone for 7 days based on decidualisation marker expression.
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Project description:Endometrial cancer (EC) is characterized by high estrogen levels unopposed by progesterone. Treatment with progestins is standard for early EC, but response to progestins is dependent on progesterone receptor (PGR) expression. Here, we show that the expression of PGR in endometrial epithelial cells is dependent on ARID1A, a DNA-binding subunit of the SWI/SNF chromatin remodeling complex that is commonly mutated in EC. In endometrial epithelial cells with estrogen receptor overexpression, we find that ARID1A promotes estrogen signaling and regulates common gene expression programs. Normally, endometrial epithelial cells expressing estrogen receptor respond to estrogen by upregulating the PGR. However, when ARID1A expression is lost, upregulation of PGR expression is significantly reduced. This phenomenon can also occur following loss of the SWI/SNF subunit BRG1, suggesting a role for ARID1A- and BRG1-containing complexes in PGR regulation. We find that PGR is regulated by a bivalent promoter, which harbors both H3K4me3 and H3K27me3 histone tail modifications. H3K27me3 is deposited by EZH2, and inhibition of EZH2 in the context of ARID1A loss results in restoration of estrogen-induced PGR expression. Our results suggest a role for ARID1A deficiency in the loss of PGR in late-stage EC, and a therapeutic utility for EZH2 inhibitors in EC.
2022-03-14 | GSE195503 | GEO
Project description:The ESR1 Cistrome in human endometrial biopsies was characterized and compared to gene regulations between the proliferative and mid-secretory pahses to infer estrogen target genes. ESR1 and PGR cistromes and 3D-cjromatin structures in cultured endometrial biopsies were characterized and compared to gene regulations induced by estrogen or progesterone in comparison to the whole endometrium.
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Project description:This SuperSeries is composed of the following subset Series: GSE29435: Progesterone inhibits epithelial-to-mesenchymal transition in endometrial cancer: cell line data GSE29436: Progesterone inhibits epithelial-to-mesenchymal transition in endometrial cancer: patient data Refer to individual Series
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Project description:TRIM28 interacts with PGR and ESR1 in both human and mouse uterus to modulate estrogen and progesterone signaling. Knocking down of TRIM28 in the human endometrial stromal cells impaired decidualization in vitro. Deletion of TRIM28 from mouse uterus disrupted uterine stromal decidualization leading to infertility. Additionally, TRIM28 deletion caused abnormal accumulation of TRIM28 positive and PGR negative cells in the stroma.
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Project description:Progesterone signaling in endometrial epithelial organoids
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